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86 Evolution News Articles
for October 2020
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10-30-20 How two immune system chemicals may trigger COVID-19’s deadly cytokine storms
A study in mice hints at drugs that could be helpful in treating severe coronavirus infections. Exactly how the coronavirus kills is a mystery. But part of the problem may be a partnership between just two immune system chemicals that triggers deadly organ damage. In mice, a combination of immune chemicals called TNF alpha and gamma interferon trips a domino chain of biochemical reactions that ultimately leads to three types of cell death, researchers report October 29 at bioRxiv.org. That wave of cell death further feeds an escalation of immune chemicals, known as a cytokine storm, that leads to more cell death and causes tissue and organ damage and failure. If the same process happens in people with severe COVID-19, the research points to several existing drugs that might help calm the cytokine storm and prevent severe disease or aid recovery. The preliminary results, however, have not yet been reviewed by other scientists. Study after study has found that people with severe COVID-19 have elevated levels of inflammation-stimulating chemicals called cytokines in their blood compared with healthy people, says immunologist Thirumala-Devi Kanneganti of St. Jude Children’s Research Hospital in Memphis, Tenn. But the mechanism by which cytokines can lead to organ failure and death isn’t known. Kanneganti and colleagues selected eight of the most commonly elevated cytokines in severely ill COVID-19 patients to see how the cytokines affect cells growing in lab dishes. Alone, none of cytokines caused harm to infection-fighting macrophage cells. But when the researchers treated macrophages with a cocktail of all eight cytokines, “we were seeing dramatic cell death, unbelievable, through the roof,” Kanneganti says. The team then tried various combinations of cytokines and discovered that only the pairing of TNF alpha and gamma interferon was deadly to macrophages.

10-30-20 Viruses have been shown to produce their own energy for the first time
A few giant viruses appear to generate their own energy, which viruses aren’t supposed to be able to do. The finding will fuel an already fierce debate about whether giant viruses really are viruses, and if they are alive or not. “It is really incredible to have energy in a virus,” says Bernard La Scola at Aix-Marseille University in France. Why any virus needs to produce its own energy remains a mystery, he says. Up until 2003, all known viruses consisted of nothing more than RNA or DNA wrapped in a protein coat or membrane. These have no working machinery inside them and are reliant on cells they infect to copy themselves. Under many definitions of life, they aren’t alive. But in 2003, La Scola reported the discovery of the first giant virus, called mimivirus. Since then, hundreds more giant viruses have been discovered and the division between viruses and living cells has become blurred. Some giant viruses are bigger than some bacterial cells, and have large genomes with lots of genes. They have some machinery to copy DNA into RNA on their own, which is unusual for viruses. They can get attacked by smaller viruses and have a kind of immune system. “Twenty years after the discovery of the mimivirus, all the definitions of a virus are no longer true,” says La Scola. He and his colleagues have now found that some giant viruses called pandoraviruses generate a membrane potential – an electrical gradient – across their outer membrane. It takes energy to generate a membrane potential, and since these are present in isolated viruses as well as in those inside cells, that energy must come from the virus itself, says La Scola. Why they have membrane potentials is still unclear. In most cells, these drive the production of a molecule called ATP, but the viruses don’t make ATP.

10-30-20 These human nerve cell tendrils turned to glass nearly 2,000 years ago
Part of a young man’s brain was preserved by hot ash from Mount Vesuvius’ A.D. 79 eruption. Nearly 2,000 years ago, a cloud of scorching ash from Mount Vesuvius buried a young man as he lay on a wooden bed. That burning ash quickly cooled, turning some of his brain to glass. This confluence of events in A.D. 79 in the town of Herculaneum, which lay at the western base of the volcano, preserved the usually delicate neural tissue in a durable, glassy form. New scrutiny of this tissue has revealed signs of nerve cells with elaborate tendrils for sending and receiving messages, scientists report October 6 in PLOS ONE. That the young man once possessed these nerve cells, or neurons, is no surprise; human brains are packed with roughly 86 billion neurons (SN: 8/7/19). But samples from ancient brains are sparse. Those that do exist have become a soaplike substance or mummified, says Pier Paolo Petrone, a biologist and forensic anthropologist at the University of Naples Federico II in Italy. But while studying the Herculaneum site, Petrone noticed something dark and shiny inside this man’s skull. He realized that those glassy, black fragments “had to be the remains of the brain.” Petrone and colleagues used scanning electron microscopy to study glassy remains from both the man’s brain and spinal cord. The researchers saw tubular structures as well as cell bodies that were the right sizes and shapes to be neurons. In further analyses, the team found layers of tissue wrapped around tendrils in the brain tissue. This layering appears to be myelin, a fatty substance that speeds signals along nerve fibers. The preserved tissue was “something really astonishing and incredible,” Petrone says, because the conversion of objects to glass, a process called vitrification, is relatively rare in nature. “This is the first ever discovery of ancient human brain remains vitrified by hot ash during a volcanic eruption.”

10-30-20 The first Denisovan DNA outside Siberia unveils a long stint on the roof of the world
Genetic evidence puts Denisovans on the Tibetan Plateau from 100,000 to 60,000 years ago. Mysterious, now-extinct members of the human lineage called Denisovans lived at the roof of the world for possibly 100,000 years or more. Denisovan mitochondrial DNA extracted from sediment layers in Baishiya Karst Cave on the Tibetan Plateau indicates that these humanlike folk inhabited the high-altitude site roughly 100,000 years ago and again around 60,000 years ago, say geoarchaeologist Dongju Zhang of Lanzhou University, China, and her colleagues. These are the first examples of Denisovan DNA found outside of Siberia’s Denisova Cave (SN: 12/16/19). Cave sediment possibly dating from 50,000 to 30,000 years ago also yielded Denisovan mitochondrial DNA, the scientists report in the Oct. 30 Science. If further research confirms that age estimate, it raises the likelihood that Denisovans survived on the Tibetan Plateau long enough to encounter the first humans to reach those heights as early as 40,000 years ago. In that case, ancient humans new to the region’s thin air may have acquired advantageous genetic traits for that environment by mating with resident Denisovans. Present-day Tibetans carry a Denisovan gene variant that aids high-altitude survival (SN: 7/2/14), although it’s not clear if interbreeding occurred on the Tibetan Plateau. Zhang’s group previously identified a lower jaw fossil from Baishiya Karst Cave as having come from a Denisovan that lived at least 160,000 years ago (SN: 5/1/19). That analysis focused on the jaw’s protein structure, not DNA, leaving questions about the find’s evolutionary identity. In the new study, Denisovan mitochondrial DNA at Baishiya Karst Cave — found in sediment layers that also contained stone tools and pieces of animal bones — displayed close links to mitochondrial Denisovan DNA at Denisova Cave, located about 2,800 kilometers northwest of the Tibetan Plateau site. Overall, the new findings suggest “that Denisovan populations were widespread in eastern Eurasia and had adapted to the Tibetan Plateau for a long time,” Zhang says.

10-28-20 Long covid: Why are some people sick months after catching the virus?
THE argument for naturally obtained herd immunity as a solution to the coronavirus pandemic has made a return in recent weeks. But letting the virus spread among younger people, who are less likely to die from covid-19, could lead to devastating consequences. Estimates suggest that there could already be millions of people around the world living with “long covid” – what appears to be a debilitating syndrome that follows a coronavirus infection. As personal stories of long-term problems accumulate, researchers and health bodies are learning more about what might cause these long-lasting symptoms, and how best to treat them. “I’m not sure how I caught the virus,” says Heather-Elizabeth Brown, a 36-year-old corporate trainer in Michigan who has severe symptoms six months after her initial diagnosis. “I was social distancing, staying out of crowds and wearing a mask.” Still, Brown became unwell at the start of April. After initially being dismissed by doctors, and testing negative for the coronavirus twice, Brown was admitted to hospital in mid-April, when she finally tested positive. By then, she was feverish and struggling to breathe, and chest X-rays revealed signs of pneumonia. Within a couple of days of her hospitalisation, Brown was put on a ventilator and placed in a medically induced coma for a month, she says. During that time, she developed blood clots in her legs and her brain. “It’s a miracle I survived,” she says. She isn’t out of the woods yet. There isn’t yet an official clinical definition of long covid, but a growing number of people are reporting symptoms that can last for months. Prolonged chest pains, shortness of breath and fatigue are often mentioned. Some people experience lasting damage to their heart and lungs, and blood clots that can cause painful swelling or strokes.

10-28-20 Do potatoes and tomatoes make rheumatoid arthritis worse?
Claims that solanine, a toxic compound found in many plants, exacerbates arthritis are a staple of health columns – but there’s no sound science to back this up, finds James Wong. AS A botanist fascinated by the properties of plants, I am always curious when I uncover new claims about them. So when a colleague lamented to me about having to give up eating tomatoes (her very favourite food) over lunch the other day, fearful they would exacerbate her crippling rheumatoid arthritis, I could barely clear my plate before reaching to dig out the studies. The first thing I discovered was that a link between tomato consumption and this painful, poorly understood degenerative condition wasn’t a new idea at all, just new to me that day. It has been a staple for health writers in newspapers, books and blogs for decades. It isn’t just tomatoes either. Everything in the botanical family to which they belong, called the nightshades, including potatoes, aubergines, peppers, chillies and crops such as goji berries, is claimed to exacerbate the symptoms of arthritis. The alleged culprit is a toxic alkaloid compound they apparently contain called solanine. So what does solanine do in this context? To my surprise, I couldn’t find a single scientific paper that addressed the question. In fact, to date there appear to have been no peer-reviewed clinical trials investigating if solanine even has any plausible connection with rheumatoid arthritis to begin with. The only reference I could find was an animal study in the Arab Journal of Nuclear Sciences and Applications, which involved feeding rats a special diet based largely on diseased potatoes. Potato plants produce solanine to defend themselves against pathogens, so rotting potatoes are likely to have particularly high levels of it. This study did indeed find increased levels of some blood markers associated with rheumatoid arthritis in these rats. But humans aren’t rats and we don’t eat diets based on rotting potatoes. Even if these results were transferable to humans, how do we know it was the spuds that had the effect, and not the pathogen?

10-28-20 People easily distracted by their phones perform worse on memory tests
Media multitasking, such as scrolling through social media while watching a movie, may be linked to more lapses in attention and difficulty remembering things. “Our data support the idea that we should be aware of how we engage with media,” says Kevin Paul Madore at Stanford University in California. He and his team compared people’s self-reported levels of media multitasking with their performances in a memory task, as part of a study including 80 participants aged 18 to 26. The researchers specifically tested episodic memory, which helps us recall events, by presenting the participants with images of objects on a computer and then later asking them to recall whether they had seen the objects earlier or not. At the same time, the team used EEG and eye tracking to monitor people’s attentiveness. Madore and his colleagues also asked participants to complete a questionnaire to determine how often they engage in various forms of media multitasking, such as texting while watching TV or reading while listening to music. They found that people who reported more frequent media multitasking had more lapses in attention during the memory task, which was associated with increased difficulties with remembering. “I think conscious awareness of attentiveness and limiting potential distractions can go a long way in memory preparedness and reducing mind wandering or mind blanking,” says Madore. “Resisting media multitasking during school lectures or work zooms, or limiting media multitasking to set times, could be valuable.” “Media multitasking is becoming more prominent. We don’t actually know anything about the effects yet,” says Amy Orben at the University of Cambridge. “In a lot of technology studies we ask people, ‘How many hours do you spend doing x?’, ‘How many hours do you spend on social media?’, ‘How many hours do you spend gaming?’, and we don’t capture a lot of the times when they co-occur.”

10-28-20 Why you probably aren't as moral as you think you are
Thanks to virtual reality, we can run experiments that test what people will do in situations where lives are on the line. We often find people act against what they claim to regard as morally acceptable, says Sylvia Terbeck. YOU probably aren’t as moral as you think. Philosophers have often asked people how they would act in a given situation when lives are on the line, but it is hard to test what they would do in practice. Now, thanks to virtual reality, we are starting to find out – and what people say doesn’t match up with what they do. There are many thought experiments and dilemmas for breaking down ethical decisions, and perhaps none is more famous than the trolley problem. The scenario begins with a runaway trolley that is on course to kill five railway workers who are stuck on the tracks. You can divert it by flipping a switch, which would kill one railway worker on an alternative track but save the other five. Is it morally acceptable to flip the switch? Most people say yes. Now imagine the same situation, but this time you are standing on a footbridge over the tracks. To save the five workers, you would need to push a stranger off the bridge to stop the trolley, killing them but saving the five. Is that morally acceptable? In this case, most people say no, even though one person is killed to save five in both scenarios. The trolley problem was developed by Philippa Foot, a philosopher and fellow of the British Academy born 100 years ago this month. Many studies have looked into why we find such a difference in moral intuitions between the two cases it describes. Some researchers have suggested that people might be unwilling to push the man because of empathic concern about his situation. My colleagues and I have studied people’s behaviour in this dilemma by immersing them in virtual reality. In one such experiment, we put 100 people into a simulated version of the trolley problem.

10-28-20 What can we learn from failed attempts to change people's behaviour?
A study of interventions aimed at changing people’s behaviour suggests that those that fail have common features. Identifying these features could help predict potential ways in which future interventions might fail and provide an opportunity to prevent this, says Magda Osman at Queen Mary University of London. Osman and her colleagues analysed 65 articles published between 2008 and 2019, which identified failed behavioural interventions, including nudges – subtle suggestions aimed at influencing people’s behaviour. They found that behavioural interventions that relied on social comparisons and social norming, for instance encouraging people to adopt a behaviour by indicating that it is a common or normal behaviour in society, accounted for the majority – 40 per cent – of the failed interventions studied. Other strategies that appeared among the failed interventions included those that delivered messages via letters or texts (24 per cent) or through labelling on products (12 per cent), and those that relied on defaults, such as opt-in or opt-out strategies (15 per cent). The researchers also categorised various ways in which interventions failed, such as by producing no effect at all or by backfiring and producing an unwanted side effect. Considering both the type of behavioural intervention as well as potential ways interventions may fail in advance could help with the design of more successful interventions, says Osman. Osman and her team are developing models that could help predict how a given behavioural intervention might perform, based on their analysis of failed interventions. “You can simulate different outcomes before you start running a behavioural intervention that might fail”, which could save time and money, she says.

10-27-20 Mummified llamas yield new insights into Inca ritual sacrifices
The animals were bound, decorated and probably buried alive. Mummified llamas stashed at a more than 500-year-old site on Peru’s southern coast offer the first direct glimpse of Inca ritual sacrifices of these animals. Colored strings made from the hair of llamas or closely related animals decorated five naturally mummified llamas found at an Inca administrative center called Tambo Viejo. Four of those llamas lay together beneath the floor of a large, rectangular structure, Lidio Valdez, an archaeologist at the University of Calgary in Canada, and his colleagues report in the December Antiquity. Scattered remains of at least three more llamas were found near the intact animals. Another llama, missing its head and possibly moved from another location, had been placed under the floor of a smaller building. Bones of hundreds of llamas had already been found at Tambo Viejo, consistent with Spanish historical accounts of mass llama sacrifices to appease various Inca deities. Those ceremonies involved the slaughter of llamas that were probably butchered and eaten, not interred whole, Valdez’s group says. The newly discovered llamas were killed as youngsters, bound and likely buried alive (along with live guinea pigs) as part of an event held to win support from local residents for Inca annexation of the region (SN: 10/6/11), the scientists say. Lab exams detected no cuts to llamas’ throats or midsections. Llama sacrifices occurred in front of local audiences, Valdez and his colleagues speculate. Large ovens and remains of partly burned animal bones and sweet potatoes at Tambo Viejo fit a scenario in which public feasts followed ritual sacrifices. Archaeological evidence of Inca child sacrifices has also been found elsewhere in Peru (SN: 9/22/10). But Spanish accounts from the 1600s indicate that Inca authorities most often targeted llamas and guinea pigs as sacrificial offerings, the researchers say.

10-27-20 How malaria parasites hide from the human immune system
The parasite may turn genes on or off to allow the spleen to clean up infected blood cells. Malaria parasites survive tough times by not being too clingy. During Africa’s dry season, when mosquitoes are scarce, malaria parasites have a hard time spreading to new hosts. So the parasites hide out in the human body by keeping the cells they infect from clinging to blood vessels, researchers report October 26 in Nature Medicine. This way, infected cells get removed from circulation and parasite levels in the body remain low, making people less sick and allowing the parasite to persist undetected. Doctors have long observed that symptoms of malaria, a deadly mosquito-borne infection, tend to wane during the dry season, which runs from January to May. But the reason has been unclear. Keeping a low profile during dry months is a successful strategy for the parasite, says Martin Rono, a parasitologist at the KEMRI-Wellcome Trust in Kilifi, Kenya, who was not involved in the work. Knowing how malaria parasites persist without causing disease, until mosquitoes return to ferry the organisms from an infected person to the next victim could help efforts to control malaria during the dry season. Plasmodium falciparum, the parasite responsible for malaria, infects red blood cells as part of a complex life cycle. Once inside a cell, the parasite produces proteins that dock on the cell’s exterior and make it stick to blood vessels so that it won’t be carried to the spleen, where it would otherwise get removed from the body. Typically, only the early life stages of the parasite circulate in the blood, while older parasites thrive inside red blood cells adhered to blood vessels, says Silvia Portugal, a biologist who led the work while at Heidelberg University Hospital in Germany. “That’s textbook, so it was very surprising” to see that dry-season parasites behaved differently in the lab, she says—the cells weren’t sticking.

10-26-20 Malaria parasite hides in human blood by changing how its genes work
An estimated 200 million people a year contract malaria, and the disease killed nearly 400,000 people in 2018 alone – now we are a small step closer to understanding why it is so hard to stop. The main parasite that causes the disease has developed a strategy for hiding undetected in the bloodstream of carriers. Malaria is caused by five species of the parasite Plasmodium, the deadliest being Plasmodium falciparum. The parasite infects human red blood cells and replicates inside them, leading to symptoms including fever and muscle aches. Most cases of malaria occur during the rainy season – which in some parts of West Africa occurs between July and December. It makes good adaptive sense for P. falciparum to replicate during these months, because the mosquitoes that can spread the disease from person to person are abundant. What hasn’t been clear is how the parasite responds during the nearly six-month-long dry season, when mosquitoes are rare. Silvia Portugal at Heidelberg University in Germany and her colleagues have discovered that P. falciparum alters its gene expression in a way that helps it survive undetected in the human bloodstream, ready to flare up again when the rains return. Portugal and her colleagues followed 600 people in Mali. During the 2017 and 2018 rainy seasons, they recorded 386 and 347 respective diagnosed cases of malaria with fever. In the dry seasons, only 12 cases with fever were diagnosed in 2017, and five cases in 2018. “What the parasite has found here is kind of a sweet spot,” says Portugal. During the dry season, it remains at levels so low as to rarely cause any disease symptoms or elicit a response from the person’s immune system. To work out how the parasite does this, the researchers sampled and analysed P. falciparum collected from carriers during both the rainy and dry seasons. During the rainy season, the parasites produced a molecule that makes red blood cells more likely to stick to blood vessels. This makes the parasite-containing cells less likely to travel to the spleen, essentially a blood filter in which damaged or diseased red blood cells are removed.

10-26-20 CRISPR weapon spread by bacterial sex could destroy deadly superbugs
Bacteria armed with a CRISPR-based weapon that infects other microbes during the bacterial equivalent of sex could help us kill off dangerous antibiotic-resistant superbugs – if regulators approve their use. While the approach has huge promise, its reliance on genetically engineered bacteria is likely to be controversial. “We would be releasing genetically modified killing machines into the environment. What could go wrong?” says David Edgell at Western University in Canada. There are two main problems with conventional antibiotic drugs. First, they often kill beneficial bacteria along with dangerous ones and disrupt microbiomes. This is why a dose of antibiotics can trigger diarrhoea. Second, many bacteria are becoming resistant to the drugs, including antibiotics such as carbapenem that are regarded as one of the last lines of defence. In theory, the CRISPR gene-editing technique can solve both problems. It can be adapted to kill harmful bacteria by targeting specific DNA sequences, while leaving bacteria that lack these sequences unharmed. The main obstacle is getting DNA coding for the necessary CRISPR machinery inside bacterial cells. One way to do this is to exploit the bacterial equivalent of sex, a process called conjugation during which two bacteria link up via a narrow tube and transfer circular pieces of DNA known as plasmids. Antibiotic resistance often spreads on plasmids. Guillaume Launay at the University of Lyon, France, and his colleagues did this by creating a plasmid coding for the CRISPR machinery needed to target the genes for carbapenem resistance. They then added this targeted antibacterial plasmid to a strain of E. coli bacteria. Finally, they mixed the engineered E. coli with other bacteria, including some that were resistant to carbapenem. As they hoped, the carbapenem-resistant bacteria were eliminated from the mix.

10-26-20 The longest trail of fossilized human footprints hints at a risky Ice Age trek
The nearly 1.5-kilometer-long trail was made by a young adult carrying a toddler. On a day during the late Ice Age, a young adult or teen carrying a toddler hustled across a muddy flat where mammoths and giant sloths roamed. Now, over 10,000 years later, fossilized footprints reveal that possibly perilous journey. The tracks, found in New Mexico’s White Sands National Park, stretch for nearly 1.5 kilometers across the plain and back, making them the longest set ever found, researchers report in the Dec. 1 Quaternary Science Reviews. “The length of the trackway is really exceptional and give us a prolonged window into the behavior of the individuals,” says evolutionary biologist Kevin Hatala of Chatham University in Pittsburgh, who was not involved in the research. It evokes a personal and intimate connection with our ancestors, as many people today can relate to the feeling of holding a child in their arms, he says. Scientists stumbled across the find when, in 2018, they spied a continuous stretch of dark spots along what was once the shore of the ancient Lake Otero, now dried up. A little digging revealed fossilized human footprints as well as those from a mammoth and ground sloth. Of the 427 human footprints discovered, researchers analyzed 90. The size and the depth of the footprints suggest that they had been made by a teen or a young woman, the researchers say. Uneven prints hint that the surface was slippery and that on one leg of the journey, the person at times shifted a heavy load. That load appeared to be a child: Smaller prints from perhaps a 3-year-old appeared next to the larger footprints in several spots. “It looks like the person was in a hurry, we don’t know why. It was a fast walk and looks like the person was tired… but kept going,” says David Bustos, a biologist at the White Sands National Park.

10-23-20 Record $8 billion payout won’t turn back the clock on US opioid crisis
A long-running lawsuit against a pharmaceutical company accused of fuelling the US opioid addiction crisis was settled this week when Purdue Pharma agreed to pay out $8.3 billion, the largest ever such settlement. The firm admitted to violating anti-kickback laws, conspiring to defraud the US and to facilitating the dispensing of medication without a legitimate medical purpose. While the size of the payout may sound like a big win, it won’t reverse the US’s opioid dependency problems, nor is it likely to be sufficient deterrent to similar behaviour by drug firms in future, say critics. No individuals from the company and none of the Sackler family owners have been convicted as part of the settlement, but a criminal investigation into individuals is ongoing. “Criminal charges against corporations don’t work. They’re seen by companies as the cost of doing business,” says Andrew Kolodny at Brandeis University in Massachusetts. Doctors used to be highly cautious about giving opioids, the most potent class of painkillers, reserving them for severe short-lasting pain like that from surgery, or for people with terminal cancer. In the 1990s, US doctors started prescribing them more liberally, spurred in part by Purdue’s marketing of a new opioid OxyContin, which the firm claimed rarely caused dependence. The firm promoted the product heavily to some doctors with free trips and paid speaking engagements. But OxyContin can lead to addiction, and some users sought ever-increasing doses. Over time, some people switched to using illegally bought pills or injecting heroin. Deaths caused by opioid overdoses climbed from about 9000 a year in 2000 to 47,000 a year in 2017, although such fatalities may now be plateauing. The astonishing number of fatal drug overdoses may have even lowered life expectancy in the US.

10-23-20 Covid-19 news: Blood plasma therapy has limited effect, study finds
The latest coronavirus news updated every day including coronavirus cases, the latest news, features and interviews from New Scientist and essential information about the covid-19 pandemic. Study finds convalescent plasma treatment is of limited benefit in covid-19. Transfusions of plasma from people who have recovered from covid-19 offer limited benefit in terms of saving lives or reducing the severity of illness, a study has found. Convalescent plasma – a component of blood from people who have recovered from covid-19 – is being collected by NHS Blood and Transplant for use in studies in the UK, and was granted an emergency use authorisation by the US Food and Drug Administration (FDA) in August, despite limited evidence that it had an effect. Convalescent plasma was used as a treatment for more than 100,000 patients admitted to hospital with covid-19 in the US between April and August. Tests for the coronavirus in sewage are being used to try to predict where new outbreaks might occur. A sewage sampling programme has been piloted in the south-west of England since June, and has already detected a spike in cases in the region and alerted NHS Test and Trace, according to the UK government. The programme is now being rolled out across more than 90 wastewater treatment sites in the UK, which cover about 22 per cent of the population of England. The antiviral drug remdesivir has been approved by the FDA as a treatment for people hospitalised with covid-19, despite a recent World Health Organization study suggesting it has little effect on survival in covid-19. It is the first drug in the US to receive approval for the treatment of covid-19. Travellers returning to Australia may soon be allowed to opt to be put under surveillance through a smartphone app or a wearable tracking device so they can quarantine at home, rather than in a hotel, a government review suggests.

10-23-20 CRISPR turns normal body fat into a type that burns energy
.Metabolic conditions linked to obesity could be treated by removing fat from a person, turning it into energy-burning “beige fat” using CRISPR gene editing and then implanting the altered fat back into the body, animal studies suggest. “It would be a personalised therapy for metabolic disease,” says Silvia Corvera at the University of Massachusetts Medical School. While most fat merely stores energy, some types – known as brown and beige fat – burn glucose to produce heat. People have small patches of brown fat but it only becomes active after repeated exposure to the cold. Her team previously showed that implanting extra beige fat into mice fed a high-fat diet makes them better at regulating blood sugar levels. Another team led by her colleague Michael Czech has shown that normal fat can be turned into what appears to be beige fat by switching off a gene called NRIP1. Read more: Grow fat, get thin? We put brown fat to the test. Now the two teams have joined forces. The researchers used CRISPR genome editing to deactivate the NRIP1 gene in human fat precursor cells, which then gave rise to beige fat cells. They then implanted these cells into mice. When the animals were put on a high-fat diet, those implanted with the human beige fat put on almost half as much weight as those implanted with unedited human fat. Those given beige fat also continued to regulate blood sugar normally, whereas those with normal fat became glucose intolerant. Around a gram of fat from a person would provide enough fat precursor cells for the treatment, says Corvera. The method will need to be tested in non-human primates before being tried in humans.

10-23-20 Covid: US gives full approval for antiviral remdesivir drug
US regulators have given full approval for the antiviral drug remdesivir to treat Covid-19 patients in hospitals. The US Food and Drug Administration (FDA) said Veklury, the drug's brand name, cut the recovery time on average by five days during clinical trials. "Veklury is the first treatment for Covid-19 to receive FDA approval," the FDA said in a statement. The World Health Organization (WHO) said last week remdesivir had little to no effect on patients' survival. The WHO said this was based on its own study - but the drug's manufacturer Gilead rejected the findings of the trial. Remdesivir had been authorised for emergency use only in the US since May. In the US it will cost $3,120 via private insurers and $2,340 via government purchasers for a five-day course. It was recently given to President Donald Trump after he tested positive for Covid-19. He has since recovered. In the statement, the FDA said the drug was approved on Thursday "for use in adult and paediatric patients 12 years of age and older and weighing at least 40 kilograms (about 88 pounds) for the treatment of Covid-19 requiring hospitalisation". "Today's approval is supported by data from multiple clinical trials that the agency has rigorously assessed and represents an important scientific milestone in the Covid-19 pandemic," said FDA Commissioner Stephen Hahn. The regulator said its decision was supported by the analysis of data from "three randomised, controlled clinical trials that included patients hospitalised with mild-to-severe Covid-19". One of the studies showed that that "the median time to recovery from Covid-19 was 10 days for the Veklury group compared to 15 days for the placebo group". For its Solidarity clinical trial, the WHO tested the effects four potential treatments - remdesivir was one, but they also looked at malaria drug hydroxychloroquine, auto-immune drug interferon, and the HIV drug combination of lopinavir and ritonavir. Dexamethasone, a low-cost steroid now widely used on Covid patients in intensive care in the UK, was not included in this study. The four drugs were tested with 11,266 adult patients in total, across 500 hospitals in more than 30 different countries. The results, which are yet to be peer-reviewed, suggested that none of these treatments had a substantial effect on mortality or on the length of time spent in hospital, the WHO said.

10-23-20 The arthritis drug tocilizumab doesn’t appear to help fight COVID-19
Additional clinical trials are still assessing the anti-inflammatory drug. An initial crop of clinical trials testing an anti-inflammatory drug against COVID-19 do not look promising. The best available evidence among these trials “doesn’t show that this drug is beneficial,” says Adarsh Bhimraj, an infectious diseases physician at the Cleveland Clinic, who was not involved in the research. The drug, tocilizumab, is a treatment for the painful joint swelling that occurs in rheumatoid arthritis and is also used to manage a dangerous side effect of the cancer treatment CAR-T cell therapy (SN: 6/27/18). So clinical trials have been assessing whether tocilizumab might help COVID-19 patients by taming excessive inflammation as it does for these other two conditions. The drug works by blocking the activity of a protein called interleukin 6, which contributes to the immune system’s inflammatory response. High levels of this protein, known as a cytokine, are a harbinger of severe disease in COVID-19 patients, studies have found. Of the four clinical trials that have just reported peer-reviewed results on tocilizumab for COVID-19, only one meets the “gold standard” for evaluating a drug. Such randomized, double-blinded controlled trials randomly assign patients to receive a drug or a placebo, and don’t reveal to participants or doctors who is getting which. In the trial with this design, tocilizumab did not reduce the risk of intubation or death as of four weeks compared with the placebo, researchers reported online in the New England Journal of Medicine on October 21. The study included 243 participants hospitalized with COVID-19 at seven Boston hospitals. Two-thirds received the drug, while the remainder received the placebo; participants also got other available drugs for COVID-19, such as remdesivir (SN: 5/13/20).

10-23-20 Bat-winged dinosaurs were clumsy fliers
Yi and Ambopteryx were a dead end on the evolutionary road to bird flight. Only two dinosaur species are known to have had wings made out of stretched skin, like bats. But unlike bats, these dinos were capable of only limited gliding between trees, a new anatomical analysis suggests. That bat-winged gliding turned out to be a dead end along the path to the evolution of flight, researchers say. “They are a failed experiment,” says Alexander Dececchi, a paleontologist at Mount Marty University in Sioux Falls, S.D. Fliers with feathered wings, rather than membranous wings, begin to appear in the fossil record just a few million years after the bat-winged dinosaurs. Those feathered fliers may have outcompeted the gliders in their evolutionary niche, Dececchi and colleagues suggest October 22 in iScience. Yi qi and Ambopteryx longibrachium were crow-sized dinosaurs that lived about 160 million years ago (SN: 4/29/15). They were distant cousins, both belonging to a bizarre group of dinosaurs known as scansoriopterygids. Unlike other scansoriopterygids, however, these two species sported large wings with membranes, thin skin stretched between elongated arm bones. Scansoriopterygids were a branch of theropod dinosaurs, the same group that includes giants like Tyrannosaurus rex as well as the ancestors of birds. So the recent discoveries of two different bat-winged theropod dinosaurs shook up long-standing ideas about the evolution of flight in birds. Scientists had thought that path, while a bit circuitous, centered around variations of just one basic, birdlike body plan. But whether Yi and Ambopteryx were actually adept at flying, such as being able to launch from the ground or flap their wings, wasn’t clear. To assess the dinos’ flight capability, Dececchi and colleagues used laser-stimulated fluorescence imaging, which can pick up details of soft tissues such as membranes or cartilage in fossils, to reanalyze the anatomy of Yi and Ambopteryx. The team made new estimations of the reptiles’ weight, wing shape and wingspan, and then simulated how those features might translate into flapping, gliding or launching.

10-22-20 The first flying dinosaurs were a failed evolutionary experiment
The first dinosaurs to take to the air were a failed evolutionary experiment. They had wings made of a skin membrane, similar to bats, but they were bad at flying and were soon outcompeted by birds. “They were badly designed gliders,” says Alex Dececchi at Mount Marty University in South Dakota. “They got squeezed out.” Birds evolved from dinosaurs, and it used to be thought they were the only evolutionary branch to gain the ability to fly. But in 2015, Xing Xu of the Institute of Vertebrate Paleontology in Beijing reported his team’s discovery of a bizarre fossil dubbed Yi qi, meaning “strange wing” in Mandarin Chinese, with wings made of a bat-like membrane, rather than feathers. In 2019, a team including Xu unveiled a fossil of another membrane-winged species called Ambopteryx longibrachium. Now, a team including Dececchi and Xu have done a more detailed study of the flying abilities of these animals, based partly on laser scans of the Yi fossil, that have revealed more details about their soft tissues. It still isn’t clear exactly what shape the wings were, however, so the team looked at several arrangements. One possibility is these animals had wings shaped like a bat’s, connected to the legs. Another is that they were shaped more like those of birds. It was most likely something in-between these, the team thinks. The findings suggest that Yi and Ambopteryx were not only incapable of powered flight, as previously thought, but they weren’t even as good at gliding as some modern animals like flying squirrels. This means they were almost certainly tree-dwelling animals that only glided short distances, the team believes. At the time that Yi and Ambopteryx evolved around 160 million years ago, there were no birds and the skies were dominated by relatively large pterosaurs, a separate group to dinosaurs. But once birds evolved a few million years later, membrane-winged dinosaurs had nowhere to go, in evolutionary terms.

10-22-20 Llamas may have been buried alive in ritual sacrifice by the Incas
The remains of five llamas that may have been ritually sacrificed by Incas have been found in Peru. It isn’t clear how the animals were killed, but it may have been a slow death. “I have no way to prove it, but I think they were buried alive,” says Lidio Valdez at the University of Calgary in Canada. He says the llamas don’t have injuries like knife wounds to their throats, which would point to different methods of killing. The Inca Empire dominated western regions of South America for several hundred years, until Spain invaded in the 1500s. The Inca never invented the wheel and many other seemingly key technologies, but nevertheless built an advanced society. Llamas were central to their success. “They were the single most important animal,” says Valdez, providing transport, skin, fibre, fertiliser and meat. “In addition to that, the Incas believed llamas were sacred animals.” Spanish people who came into contact with the Inca reported that they regularly killed hundreds of llamas, either for feasts or for ritual sacrifices to deities. However, while archaeologists have found many examples of llamas that were killed and then eaten, llamas that were ritually sacrificed haven’t been found before. Valdez and his colleagues found five such llamas in an Inca settlement called Tambo Viejo in the Acari Valley, near the coast of Peru. The site had previously been looted, so Valdez suspects there were originally more. The llamas had no injuries, but their legs were securely tied together. Valdez suspects this was done to keep them under control while they were buried alive. He says this method of sacrifice fits with what we know about Inca practices. “Incas used to sacrifice children, and it is said some of the children were buried alive,” says Valdez, referring to written accounts from Spanish conquistadors. “If they did that with children, I’m sure they would have done the same thing with llamas.”

10-22-20 Homo erectus, not humans, may have invented the barbed bone point
An 800,000-year-old tool may be the oldest known of its kind. A type of bone tool generally thought to have been invented by Stone Age humans got its start among hominids that lived hundreds of thousands of years before Homo sapiens evolved, a new study concludes. A set of 52 previously excavated but little-studied animal bones from East Africa’s Olduvai Gorge includes the world’s oldest known barbed bone point, an implement probably crafted by now-extinct Homo erectus at least 800,000 years ago, researchers say. Made from a piece of a large animal’s rib, the artifact features three curved barbs and a carved tip, the team reports in the November Journal of Human Evolution. Among the Olduvai bones, biological anthropologist Michael Pante of Colorado State University in Fort Collins and colleagues identified five other tools from more than 800,000 years ago as probable choppers, hammering tools or hammering platforms. The previous oldest barbed bone points were from a central African site and dated to around 90,000 years ago (SN: 4/29/95), and were assumed to reflect a toolmaking ingenuity exclusive to Homo sapiens. Those implements include carved rings around the base of the tools where wooden shafts were presumably attached. Barbed bone points found at H. sapiens sites were likely used to catch fish and perhaps to hunt large land prey. The Olduvai Gorge barbed bone point, which had not been completed, shows no signs of having been attached to a handle or shaft. Ways in which H. erectus used the implement are unclear, Pante and his colleagues say. This find and four of the other bone implements date to at least 800,000 years ago, based on their original positions below Olduvai sediment that records a known reversal of Earth’s magnetic field about 781,000 years ago. Another bone artifact dates to roughly 1.7 million years ago, the researchers say.

10-22-20 How environmental changes may have helped make ancient humans more adaptable
A sediment core traces 1 million years of ecological shifts in eastern Africa. An unforgiving environmental twist deserves at least some credit for the behavioral flexibility that has characterized the human species since our African origins around 300,000 years ago, a new study suggests. For hundreds of thousands of years in parts of East Africa, food and water supplies remained fairly stable. But new evidence shows that starting about 400,000 years ago, hominids and other ancient animals in the region faced a harsh environmental reckoning, says a team led by paleoanthropologist Rick Potts of the Smithsonian Institution in Washington, D.C. The climate began to fluctuate dramatically. Faults caused by volcanic eruptions fractured the landscape and reduced the size of lakes. Large animals died out and were replaced by smaller creatures with more diverse diets. These changes heralded a series of booms and busts in the resources hominids needed to survive, Potts and his colleagues report October 21 in Science Advances. Around that time, hominids at a site called Olorgesailie in what’s now Kenya transformed their culture. That shift, between around 500,000 and 320,000 years ago, was probably influenced by increasingly unpredictable periods of water and food scarcity, the scientists contend. Stone hand axes and other cutting tools made of local stone had dominated African toolkits for 700,000 years before that transition occurred. After that, Middle Stone Age tools, such as spearpoints made from rock imported from distant sources, gained popularity, Potts’ team has previously found (SN: 3/15/18). Middle Stone Age tools were smaller and more carefully crafted implements. Widely scattered hominid groups began to trade with one another to obtain suitable toolmaking rock and other resources.

10-22-20 Dinosaur fossil with preserved genital orifice hints how they mated
A fossil dinosaur originally discovered in northwestern China is so exquisitely preserved that the shape of its cloaca – the opening used for excretion and mating – is visible for the first time. The evidence has actually been in plain sight. The psittacosaurus – a kind of early ceratopsian related to Triceratops that lived around 120 million years ago – has been on public display at the Senckenberg Museum of Natural History in Frankfurt, Germany, for over a decade and several scientific papers have already been written about its primitive feathers and colouring. Only now, though, has a team led by Phil Bell at the University of New England in Australia formally described the cloaca. Bell declined to discuss the finding until the paper is published in a peer-reviewed journal. Birds and reptiles have a cloaca – a single orifice used for excretion, urination, mating and laying eggs – so it has always been assumed that dinosaurs had them too. The cloaca of the psittacosaurus confirms this expectation. Only the external part of the cloaca has been preserved. The vent is around 2 centimetres long, is flush with the surrounding area rather than protruding as some cloacas do, and is surrounded by darkly pigmented tissue (see picture, above). The internal anatomy has not been preserved, so the fossil doesn’t definitively resolve questions about how dinosaurs mated. However, the cloaca has a longitudinal opening like those of crocodiles, which do have penises. By contrast, most birds – the living descendants of dinosaurs – do not. “It is a triumph of discovery to have such a delicate region so perfectly preserved in a fossil so old,” says John Long of Flinders University in Australia, who wasn’t involved in the research. “We have various other different parts preserved but not a cloaca.” Unfortunately, it doesn’t reveal much. It isn’t possible to tell the sex of this particular animal, but the cloaca’s resemblance to those of crocodiles suggests that this type of dinosaur had a penis.

10-21-20 We must hold a steady course on our response to covid-19
EARLY on in the pandemic, we heard a lot about behavioural fatigue – the hunch that people would quickly grow tired of restrictions on their lives and throw caution to the wind. It was a factor in the reluctance of the UK government to go into lockdown too quickly, a delay that led to the virus getting out of hand. We don’t hear very much about behavioural fatigue any more. We feel it. The prospect of further restrictions or even “circuit breaker” lockdowns (see “Should we plan for regular ‘circuit-breaker’ coronavirus lockdowns?”) is greeted with dread, and the very real possibility of disobedience. This isn’t the time to let our guard down. Two obvious reasons are that we don’t want to overwhelm hospitals or shut schools. But there is another reason to mask up, observe distancing and stick to any extra rules that apply: to prevent the virus from evolving. Up to now, we have been lucky on this score. SARS-CoV-2 has changed little since it emerged. It is so stable genetically that drugs and vaccines in development ought to work against all variants currently circulating (see “Is the coronavirus evolving and will it become more or less deadly?”). Yet we cannot take that for granted. The virus does have the capacity to mutate into something worse, but can only do so if it is transmitted from human to human. Cutting off transmission is therefore vital while we await a vaccine. If and when that vaccine arrives, high levels of uptake are vital for the same reason. Even more so, in fact, as the vaccine will put pressure on the virus to mutate. Fatigue is also partially responsible for the enthusiastic welcome that the herd immunity strategy, or “letting the virus rip”, has received in some circles. It undeniably has a certain freedom-loving appeal. Unfortunately, it is bad science (see “It is bad science to say covid-19 infections will create herd immunity”), and would also expose us to the risk of viral evolution. Risk is something we are notoriously bad at assessing. This pandemic has brought new challenges for individuals in balancing the risks to themselves and others, and for governments in balancing the needs of different sectors of society (see “Your covid-19 risk: How to navigate this new world of uncertainty”). But the behavioural fatigue fiasco showed the danger of basing policy on plausible-sounding hunches. We must not make that mistake again.

10-21-20 You can manage your covid-19 risk by setting your own ‘contact budget’
When it comes to covid-19, we all have different levels of risk we're comfortable with. Setting a weekly "contact budget" can make it easier to decide which risks are worth taking, says epidemiologist Eleanor Murray. Eleanor Murray: Back in March and April, most people had clear guidance about what they were allowed to do, and it wasn’t very much. That made life somewhat unpleasant, but it also made life easy. When things started opening up, everybody had to make their own decisions about what they are comfortable with and what might be risky. The way I was thinking about it is that there is a level of risk I am comfortable with. If I go to a grocery store during a really crowded time, to keep my average risk level constant, I’m probably not going to do something risky the next day. We are all familiar with the idea of financial budgeting, it is easy to translate to this situation. There are four metrics to keep in mind. First is how much risk you can tolerate. If you or someone in your household has a medical condition, then your tolerance is going to be lower. Next is how comfortable you are knowing that you could get infected and transmit that infection. That’s something we don’t talk a lot about, but people have told me how guilty they felt afterwards. The last two pieces are the amount of contact we need for our job and for our mental health. If you are a healthcare worker or grocery store clerk, a certain amount of contacts are required as part of your job. Then there are contacts that you need for emotional reasons. It could be really important to you to deliver groceries to your elderly neighbour or to attend a religious service. Think of person, place, time and space. “Person” is about how many people are there, and how many you are in regular contact with. The less regular contact you have, the more potential for expanding your infection network. “Place” is about whether something is inside or outside, whether it is crowded, and the risks associated with that location. “Time” is the duration you’ll be there. And “space” is whether the location is well ventilated and how well you can maintain masks and physical distancing. Whether necessary or optional, how do you make an activity as low risk as possible? Can you eat outside or get takeaway instead? Could you get the same benefit virtually?

10-21-20 Viruses have busy social lives that we could manipulate to defeat them
The coronavirus and others are no lone wolves, they cooperate and compete with one another. Understanding these social interactions could help us fight them. IF YOUR social life has suffered during the coronavirus pandemic, you may not want to know that the virus has a social life too. And it is probably better than yours right now. It may seem odd to say that viruses fraternise when they arguably aren’t even alive, but virologists are discovering just how rich this aspect of their existence is. Far from being lone operators, viruses cooperate and compete with one another; they can be altruists, freeloaders or cheats. These discoveries are rewriting the virus rule book and suggesting novel ways to tackle viral diseases, and that includes the newest one, covid-19, caused by SARS-CoV-2. Understanding these complex and sometimes strange interactions could be the key to getting our own lives back to normal. The classical view of a viral infection doesn’t create much opportunity for social interaction. A single virus particle, or virion, encounters a target cell and breaks and enters. Once inside, it disassembles like a cat burglar unpacking tools and then executes its potentially deadly genetic program. This program is designed to do one thing: build an army of virus clones to move on to the next victim. To this end, the virus requisitions the cell’s protein and genome production facilities, churning out millions of copies of its constituent parts. These viral genomes and proteins assemble into virus particles and, once they reach a critical mass, disgorge out of the host cell, killing it in the process. The infection cycle then begins anew. This view isn’t wrong, but is vastly simplified. Viral attacks are rarely solo missions. “The virion has been traditionally viewed as the minimal viral infectious unit,” says Rafael Sanjuán at the University of Valencia in Spain. “However, single virions often fail to establish productive infections.” In truth, virions usually hunt in packs, and can infect cells en masse, alongside other species of virus. And this creates hitherto underappreciated opportunities for virus-virus interactions. The microbiologists who study such interactions in the new field of sociovirology say they can be understood using the same concepts developed to describe those between animals, plants and, more recently, bacteria.

10-21-20 Long Covid: Who is more likely to get it?
Old age and having a wide range of initial symptoms increase the risk of "long Covid", say scientists. The study, seen by the BBC, estimates one in 20 people are sick for least eight weeks. The research at King's College London also showed being female, excess weight and asthma raised the risk. The aim is to develop an early warning signal that can identify patients who need extra care or who might benefit from early treatment. The findings come from an analysis of people entering their symptoms and test results into the Covid Symptom Study app. Scientists scoured the data for patterns that could predict who would get long-lasting illness. The results, which are due to be published online, show long Covid can affect anyone, but some things do raise the risk. "Having more than five different symptoms in the first week was one of the key risk factors," Dr Claire Steves, from Kings College London, told BBC News. Covid-19 is more than just a cough - and the virus that causes it can affect organs throughout the body. Somebody who had a cough, fatigue, headache and diarrhoea, and lost their sense of smell - which are all potential symptoms - would be at higher risk than somebody who had a cough alone. The risk also rises with age - particularly over 50 - as did being female. Dr Steves said: "We've seen from the early data coming out that men were at much more risk of very severe disease and sadly of dying from Covid, it appears that women are more at risk of long Covid." No previous medical conditions were linked to long Covid except asthma and lung disease. The precise symptoms of long-Covid vary from one patient to the next, but fatigue is common. Vicky Bourne, 48, started off with a fever and a "pathetic little cough" in March, which became "absolutely terrifying" when she struggled to breathe and needed to be given oxygen by a paramedic. She was not admitted to hospital, but is still - in October - living with long Covid.

10-21-20 Your covid-19 risk: How to navigate this new world of uncertainty
Baffling statistics and their impact on our emotions can make it hard to evaluate risk in this pandemic. But there are simple steps you can take to put risk in context and feel more confident in your decisions. THE covid-19 pandemic recently passed the milestone of a million deaths, and infections continue to rise. For months to come, perhaps years, we will have to keep a balance between minimising the deaths and harms caused by the coronavirus and carrying on with life to maintain our economic livelihoods and mental well-being. “Getting through this pandemic is essentially an exercise in risk management,” says Allison Schrager, an economist at the Manhattan Institute in New York. To do this well, we have to rely on the information we get from public health experts, the media and governments. We want to know how dangerous the virus is to us, and to friends or loved ones made perhaps more vulnerable by age or other factors. We want to know the risks stemming from the current surge in infection rates, so we understand whether measures such as renewed lockdowns are proportionate. Risk communication is a tricky business even at the best of times, but in many countries, the covid-19 pandemic has brought a deluge of scary-sounding statistics and graphs about infection rates and rising death tolls. David Spiegelhalter, chair of the Winton Centre for Risk and Evidence Communication at the University of Cambridge, has called it “number theatre”. So how do we take the drama out of the theatre and come to a measured assessment of the uncertainties we face? There are no easy answers, but by understanding how our brains deal with risk and the pitfalls in the way numbers concerning risk are often presented to us, we can go some way to easing the mental burden – through the pandemic and beyond. Despite nearly non-stop media coverage since the start of the year, the covid-19 pandemic remains an unfamiliar threat for most of us. This is where the difficulties with assessing its risks start. “We’re comfortable with risks we take every day, but new and dramatic ones throw us,” says Schrager.

10-21-20 Is the coronavirus evolving and will it become more or less deadly?
“FORTUNATE” isn’t a word that often comes up in relation to the coronavirus pandemic, but in one respect it is true. In the nine months that the virus behind covid-19 has been circulating widely, it has hardly mutated at all. “We are fortunate that the virus is not mutating fast,” says Sudhir Kumar at Temple University in Pennsylvania. A rapidly mutating virus could evolve into different, possibly more virulent, strains. “So it’s good to have a low diversity” among the viruses currently circulating, he says. However, this could be the calm before the storm. A recent analysis of more than 18,000 genomes of the new coronavirus, formally called SARS-CoV-2, sampled from around the world found very low levels of genetic diversity. The study, led by Morgane Rolland at the Walter Reed Army Institute of Research in Maryland, concluded that these viruses are so similar that a single vaccine should protect against them all (PNAS, doi.org/fdkz). There are three main reasons for this. First, even though SARS-CoV-2 is an RNA virus, which generally have the fastest mutation rate of any biological entity, coronaviruses change relatively slowly because their genome-copying machinery has a proofreading function. Second, when mutations have appeared, they are almost all biologically harmful or neutral to the virus, and so haven’t persisted. And third, the virus hasn’t needed to evolve in order to be successful. Not yet, anyway. This is what makes some virologists nervous as we move into the next phase of the pandemic. As a rule, evolutionary adaptation happens due to “selection pressure”, which is when an organism’s environment changes to favour certain variants over others. Right now, SARS-CoV-2 is under very weak selection pressure. There are still plenty of humans to infect who have no “immune memory” to fight the virus; there are very few drugs to evade; and there is no vaccine. But as these benign conditions become harsher for the virus, selection pressure will ramp up and we can expect to see it evolve in response, perhaps in ways that make it even more dangerous.

10-20-20 UK's vital covid-19 infection tracking survey deluged by complaints
The UK’s flagship covid-19 infection tracking survey has been deluged by complaints, with volunteers calling it an “absolute shambles”, “disappointing and frustrating” and an “utter incompetence“. Hundreds of people taking part in the Office for National Statistics’ (ONS) Covid-19 Infection Survey have taken to Twitter in the past month to register their frustration at alleged multiple problems by IQVIA, a US multinational that organises the household visits for tests to be collected. Households receive a letter inviting them to call to register for the survey, and the survey team is meant to contact them within seven days to book an appointment for a worker to visit, supervise and collect completed tests. After the first appointment, volunteers are given the option of having follow-up appointments to continue taking part in the survey. But complaints suggest this isn’t happening smoothly. Reported issues include not calling people back to book appointments, no-shows when appointments have been booked, constantly busy helplines, unanswered emails and tweets, and workers offering poor guidance on how volunteers should swab their nose and throat. The picture painted by the complaints could offer one explanation for a growing share of invited households failing to complete any tests for the survey, as New Scientist reported last week. Pete Liggins in Prestwich says the first IQVIA worker to visit him didn’t offer any advice on how to do self-swabbing tests, and it was only when he watched a video online after completing the test that he realised how to do it properly. No one called to book a follow-up appointment, and he was unable to get through to a helpline which was constantly busy. “If it’s not being carried out properly then all the sacrifices we’re being asked to make could be for nothing,” he says.

10-20-20 UK trial plans to infect volunteers with the coronavirus in January
Researchers in the UK have announced plans to infect volunteers with the coronavirus, starting in January. The initial aim will be to establish the minimum infectious dose before testing potential vaccines. The study will be funded by the UK government, but has yet to get final ethical approval. “The top priority is participants’ safety,” says Chris Chiu at Imperial College London, whose team will carry out the study. “We have spent many months thinking about the evidence and weighing up the pros and cons.” The coronavirus doses will be created by a company called hVIVO, as the research requires a pure, quantifiable source of the virus, rather than an infection spreading person to person. The doses will contain the same strain that is currently circulating and not weakened, or attenuated, in any way. Volunteers will have the virus delivered to their nose in droplets, a method widely used in previous studies of this kind. As soon they show signs of infection, they will be given the antiviral drug remdesivir. A large trial recently found that remdesivir didn’t reduce the death rate from covid-19. However, that trial involved severely ill people who had already been hospitalised, says Chiu. He thinks giving the drug very early on will stop the infection spreading to the lungs. The team will also consider using other drugs such as antibodies as more evidence becomes available. The volunteers will be healthy individuals aged between 18 and 30. Initially they are likely to be from a white ethnic background because of evidence that black, Asian and minority ethnic people are more likely to get severely ill. However, the team says it will include volunteers from more diverse backgrounds as soon as it can do so safely.

10-20-20 Fire ants build little syphons out of sand to feed without drowning
To escape a watery death, the insects construct relatively sophisticated structures on the fly. The threat of death is no obstacle for some hungry fire ants. To escape drowning while feeding on sugary water, black imported fire ants built syphons out of sand that moved the water to a safer spot. A range of animals, including birds, dolphins, primates and even ants, use objects as tools (SN: 12/30/19; SN: 6/25/20; SN: 6/24/19). Ants often employ debris or sand grains to carry food. But this is the first time that the insects have been observed adjusting their tool use to build relatively complex structures in response to a problem, researchers report October 7 in Functional Ecology. In the wild, black imported fire ants (Solenopsis richteri) typically eat honeydew produced by aphids. In the lab, entomologist Jian Chen of the U.S. Department of Agriculture’s Agricultural Research Service in Stoneville, Miss., and colleagues provided the ants with containers of sugary water. The insects have a hard, water-repellent outer covering called a cuticle, and can typically float on a liquid — and sure enough, the insects floated and fed without a problem. The researchers then reduced the water’s surface tension with a surfactant to make it more difficult for the ants to float. While some ants drowned, most stopped entering the containers and instead used grains of sand placed nearby to build structures leading from the inside of a container to outside of it. Those structures acted like syphons. Within five minutes of building one, nearly half of the water was drawn out through the sand pathway, allowing the ants to feed safely. “The fact that ants are building little syphons is new and interesting,” says Valerie Banschbach of Gustavus Adolphus College in Saint Peter, Minn., who was not involved in the study. The insects’ “flexibility to act in a creative way responding to a situation suggests that they have higher cognitive abilities than what is traditionally believed.”

10-19-20 Should we plan for regular 'circuit-breaker' coronavirus lockdowns?
With cases of covid-19 rising in most parts of the UK, there is fierce debate over the best way to respond. While some people argue for a “let the virus rip” strategy, others want increasing social restrictions, up to and including full lockdown, as happened in the pandemic’s first wave. Yet is there another way? One idea gaining ground is that countries should hold regular pre-emptive lockdowns, lasting about two weeks. They could be timed to coincide with school holidays, minimising disruption to education. In the UK, this would mean having these shut downs about every two months. The idea may sound similar to the short, sharp “circuit-breaker” lockdown, an idea advocated by some UK government scientists, including chief scientific advisor Patrick Vallance. Northern Ireland began such a lockdown on 16 October and Wales has announced it will do the same from 23 October. But there is a crucial difference between these strategies: the idea is that pre-emptive lockdowns would be planned to happen periodically, even when a country’s coronavirus case numbers are relatively low. The advance knowledge of when they are due to happen is supposed to reduce the impact on businesses, while the fact that they are short and have a definite end point could make them more bearable for the public. It is hard to work out exactly what effect this would have on virus prevalence, but it should regularly reset case numbers to a lower level. At best, it could mean avoiding the longer kind of lockdowns seen in the pandemic’s first wave. This year, there has been growing appreciation of the toll on mental health caused by stopping people mixing with their friends and family. The benefit of pre-emptive circuit breakers is that it is easier to put up with something unpleasant if you know it will be short-lived and that there is a definite end in sight. “The specified length of time reduces uncertainty, and it is uncertainty that often promotes anxiety and poor mental well-being,” says Charlotte Hilton, a chartered psychologist based in the East Midlands, UK.

10-19-20 Could cold water hold a clue to a dementia cure?
Cold water swimming may protect the brain from degenerative diseases like dementia, researchers from Cambridge University have discovered. In a world first, a "cold-shock" protein has been found in the blood of regular winter swimmers at London's Parliament Hill Lido. The protein has been shown to slow the onset of dementia and even repair some of the damage it causes in mice. Prof Giovanna Mallucci, who runs the UK Dementia Research Institute's Centre at the University of Cambridge, says the discovery could point researchers towards new drug treatments which may help hold dementia at bay. The research - although promising - is at an early stage, but it centres on the hibernation ability that all mammals retain, which is prompted by exposure to cold. There are already more than a million people with dementia in the UK and the total is expected to double by 2050. Researchers are searching for new ways to treat the condition, as current options have only limited impact. Doctors have known for decades that cooling people down can - in certain circumstances - protect their brains. People with head injuries and those who need cardiac operations are often cooled during surgery, as are babies. What has not been so well understood was why cold has this protective effect. The link with dementia lies in the destruction and creation of synapses - the connections between cells in the brain. In the early stages of Alzheimer's and other neuro-degenerative diseases, these brain connections are lost. This leads to the cascade of symptoms associated with dementia - including memory loss, confusion and mood swings - and, in time, the death of whole brain cells. What intrigued Prof Mallucci was the fact that brain connections are lost when hibernating animals like bears, hedgehogs and bats bed down for their winter sleep. About 20-30% of their synapses are culled as their bodies preserve precious resources for winter. But when they awake in the spring, those connections are miraculously reformed.

10-17-20 Remdesivir doesn’t reduce COVID-19 deaths, a large WHO trial finds
An international study found no benefit of the drug or three others. Remdesivir, an antiviral drug that was the first found to combat COVID-19, doesn’t reduce deaths from the disease, a large international study found. The World Health Organization’s Solidarity trial, which combined data from 405 hospitals in 30 countries, randomly assigned more than 11,000 people hospitalized with COVID-19 to receive one of four drugs or standard care, which could include other drugs such as steroids. The tested drugs include remdesivir, the antimalaria drug hydroxychloroquine, an anti-HIV drug called lopinavir and interferon-beta1a. Interferon is an immune system chemical that triggers the body’s antiviral defenses. None of the drugs showed any benefit in reducing deaths, the need for ventilation or the length of hospital stays, researchers report October 15 in a preliminary study posted at medRxiv.org. The work has not been vetted by other scientists yet, and some analyses may change during the peer-review process, experts say. Other studies had already shown that neither lopinavir — given in combination with ritonavir, a drug that boosts lopinavir’s levels in the body — nor hydroxychloroquine were effective against the novel coronavirus (SN: 3/19/20; SN: 8/2/20). These studies, in addition to the new data, deliver a clear message that those drugs are not helpful for treating COVID-19, says David Brett-Major, a medical epidemiologist at the University of Nebraska Medical Center in Omaha. But remdesivir has been shown to shave four days off of hospital stays in a trial conducted by the U.S. National Institute of Allergy and Infectious Diseases (SN: 4/29/20). In that study, the drug “showed a trend toward reducing deaths,” but the result wasn’t statistically meaningful. Preliminary results from small studies conducted by remdesivir’s maker, Gilead Sciences of Foster City, Calif., also suggested that drug might cut the chance of dying from the disease (SN: 7/13/20).

10-17-20 Can supplements really help fight COVID-19? Here’s what we know and don’t know
There’s little evidence yet, except maybe in people who are deficient in vitamins and minerals. Consumers have long turned to vitamins and herbs to try to protect themselves from disease. This pandemic is no different — especially with headlines that scream “This supplement could save you from coronavirus.” It also helps to have celebrity enthusiasts. When President Donald Trump was diagnosed with COVID-19, his pill arsenal included Vitamin D and zinc. And in an Instagram chat with actress Jennifer Garner in September, infectious diseases expert Anthony Fauci touted vitamins C and D as ways that might generally boost the immune system. “If you’re deficient in vitamin D,” he noted, “that does have an impact on your susceptibility to infection. I would not mind recommending, and I do it myself, taking vitamin D supplements.” But whether over-the-counter supplements can actually prevent, or even treat, COVID-19, is not clear. Since the disease is so new, researchers haven’t had much time for the kind of large experiments that provide the best answers. Instead, scientists have mostly relied on fresh takes on old data. Some studies have looked at outcomes of patients who routinely take certain supplements — and found some promising hints. But so far there’s little data from the kinds of scientifically rigorous experiments that give doctors confidence when recommending supplements. Vitamin D Why it might help: Vitamin D is a hormone building block that helps strengthen the immune system. Zinc Why it might help: It plays several supportive roles in the immune system, which is why zinc lozenges are always hot sellers in cold and flu season. Zinc also helps with cell division and growth. Vitamin C Why it might help: It’s a potent antioxidant that’s important for a healthy immune system and preventing inflammation.

10-16-20 Historical records hint daughters of older mothers may be less fertile
A study of women born in the Netherlands in the 19th century adds to the evidence that the daughters of older mothers may be less fertile. Many animal studies have found that females born to older mothers have worse health and fewer offspring on average. This could be because eggs accumulate mutations as they age. Some studies suggest the same is true of people, but in modern populations factors such as education, wealth and access to contraception have a big effect on the average number of children women have, making it hard to identify whether a mother’s age does affect her daughter’s fertility. To try to get around this, Ingrid van Dijk at Lund University in Sweden and her colleagues used data on births, deaths and marriages in the Dutch province of Zeeland during the 19th century. They looked at more than 7000 mothers, who collectively gave birth to nearly 10,000 daughters between 1812 and 1874, and who also had a collective total of just over 73,000 grandchildren born before 1914. They found that with every year’s increase in the mother’s age, there was a 0.3 per cent decrease in the number of children each daughter had. The effect is small, but statistically robust, the team says. “I think that there are some advantages to using historical populations for this type of study,” says Olga Basso at McGill University in Canada. “Women were expected to marry and have children, and most did.” This suggests childlessness was rarely voluntary, she says. By contrast, today many women choose not to have children. However, it isn’t clear that the lower number of children in daughters with older mothers in Zeeland is due solely to a biologic effect of maternal age, says Basso. For instance, the team excluded mothers who died before the age of 50, which might have biased the results.

10-16-20 The FDA has approved the first treatment for Ebola
Lab-made antibodies marshal an immune response and curb the virus’s ability to infect cells. There is now an approved treatment for Ebola, one of the world’s deadliest diseases. The U.S. Food and Drug Administration announced October 14 that Inmazeb, a cocktail of lab-made antibodies developed by the pharmaceutical company Regeneron, can be used to treat adult and pediatric patients with Ebola. The announcement comes less than a year after the FDA greenlit the first Ebola vaccine (SN: 12/20/19). “This is a big development,” says Erica Ollmann Saphire, an immunologist at the La Jolla Institute for Immunology in San Diego, Calif. Ebola virus causes severe illness, including fever, vomiting, diarrhea and bleeding. Outbreaks of the disease, discovered in the 1970s, can kill 25 to 90 percent of those infected (SN: 2/11/19). Previously, people could only be helped by supportive therapies, like replacing lost fluids, Saphire says. “But this approval means Ebola is now a treatable disease.” Inmazeb was evaluated along with three other experimental Ebola treatments in a clinical trial conducted in the Congo in 2018 and 2019 amid the second largest outbreak of the disease (SN: 8/12/19). During the trial, 33.8 percent of people treated with Inmazeb died after 28 days, compared with 51 percent of people who received a different treatment. The drug consists of three different monoclonal antibodies, human-made antibodies designed to mimic those produced naturally during an immune response. One gums up structures on the Ebola virus that allow it to infiltrate human cells, while the other two recruit immune cells to clear out the virus and infected cells. Saphire, who heads a research consortium focused on studying antibody treatments for Ebola, says that given the drug’s two-pronged approach to fighting the virus, “the Regeneron cocktail is exactly the sort of complementary approach our research predicted would be most efficacious.” (Regeneron Pharmaceuticals is a major financial supporter of the Society for Science & the Public, which publishes Science News.)

10-16-20 Minimum alcohol pricing could reduce alcohol-linked deaths in Canada
Minimum pricing for alcoholic drinks could substantially reduce hospital stays and deaths related to alcohol, a study in Canada has found. “Governments in Canada and elsewhere may consider implementing [minimum unit pricing] strategies to improve the health of drinkers and reduce alcohol’s burden on healthcare systems,” says Adam Sherk at the University of Victoria in Canada. Sherk and his colleagues analysed official data on deaths and hospitalisations related to alcohol in Quebec, Canada, in 2014, as well as information on alcohol sales and pricing in the province, which currently doesn’t have a minimum-unit-pricing policy. They then used modelling to predict the potential effects of two minimum pricing scenarios. The researchers found that a minimum unit price of CAN$1.50 (88p) per standard alcoholic drink – defined in Canada as one containing 13.5 grams of ethanol – would result in a 4.4 per cent reduction of alcohol consumption, a 5.9 per cent drop in alcohol-attributable deaths and an 8.4 per cent fall in alcohol-attributable hospital stays in Quebec. In another scenario, with a minimum unit price of CAN$1.75 (£1.03), Sherk and his team predicted that alcohol-attributable deaths in the province would be cut by 11.5 per cent and hospital stays by 16.3 per cent. Their findings are consistent with early data from Scotland, which implemented a minimum unit price of 50p per 8 grams of alcohol in 2018. The change has been linked with a reduction in weekly purchases of alcohol in Scotland. “Alcohol policies, such as minimum unit price, have particular importance during the covid-19 pandemic, as stronger alcohol policies may help to reduce the high burden on healthcare systems,” says Sherk. More than 3 million people died globally as a result of harmful use of alcohol in 2016, according to a 2018 World Health Organization report, which estimated that harmful use of alcohol causes more than 5 per cent of the world’s disease burden.

10-16-20 Boy, 12, discovers rare dinosaur skeleton
A 12-year-old boy made the discovery of his lifetime when he found a dinosaur skeleton dating back 69 million years. The amateur palaeontologist was out hiking with his father in a fossil-rich part of Alberta, Canada this July, when he saw bones protruding from a rock. On Thursday, the skeleton's excavation was completed. The boy, Nathan Hrushkin, says when he first laid eyes on the bones, he was "literally speechless". "I wasn't even excited, even though I know I should have [been]," he tells the BBC. "I was in so much shock that I had actually found a dinosaur discovery." Nathan, who has been interested in dinosaurs since he was six, often goes hiking in the Nature Conservancy of Canada's protected site in the Albertan Badlands with his father. "I've always just been so fascinated with how their bones go from bones like ours, to solid rock." A year ago, they had found small fragments of fossils, and his father guessed that they were falling down from the rock above. So this summer Nathan decided to inspect. The fossilised bones were poking out of the side of a hill. "Dad, you got to get up here!" he called to his father. His father knew Nathan had found something by the tone of his voice. "They looked like bones made of stone - you could not mistake them for anything else," his father, Dion Hrushkin, said. "It looked like the end of a femur - it had that classic bone look to it - sticking straight out of the ground." Nathan knows that the fossils are protected by law, so when they got home, he and his father logged in to the website for the Royal Tyrrell Museum, which is located in Alberta and devoted to the study of prehistoric life. The museum advised them to send photos of their discovery and its GPS coordinates, which they duly did. The Badlands are home to many fossils, and a dinosaur - named the Albertosaurus - was discovered by Joseph Tyrell in the late 1800s. But the part of the conservation site where they were walking was not known for fossil discoveries, so the museum sent a team of experts to excavate.

10-15-20 Fat stores in our cells also hold immune proteins to fight infections
Tiny fatty droplets in our cells are part of the immune system and help fight off bacterial infections. Until now the droplets were thought to be among the most vulnerable parts of the cell. Lipid droplets are found in the cells of all complex organisms. They store fats and other lipids, which are essential nutrients. In humans, specialised cells called adipocytes store body fat in the form of lipid droplets. For many years, biologists thought lipid droplets were “just an inert structure, just a storage site”, says Robert Parton at the University of Queensland in Australia. But in fact they also contain proteins, which carry out a wide range of functions. “We now have whole conferences looking just at the lipid droplets and all the associated processes.” When a bacterium infects an animal cell, it often feeds on the lipid droplets. “It’s a nice source of fat inside the cell,” says Parton. But it seems animal cells have found a way to turn the tables. “In retrospect, it sort of makes sense that in millions of years of battles between us and pathogens, the cell has also responded,” says Parton. In a series of experiments on mice and on human cells, Parton’s team found that lipid droplets carry an array of proteins that are involved in the immune response. When dangerous bacteria enter the cell, chemical alarm signals are released, and these activate the immune proteins on the lipid droplets – which kill any bacteria that approach the droplet. The cell has taken one of its most vulnerable components and weaponised it, says Parton. “It’s using it like a honey trap,” he says. “It’s producing these proteins, putting them on the lipid droplets, and then killing the bacteria.” The evidence so far only shows that the lipid droplets can fight bacteria – there is no sign of them fighting viruses.

10-15-20 Social life of extinct sabre-toothed cat revealed by ancient DNA
The first in-depth study of sabre-toothed cat DNA reveals genetic clues that some of them were swift predators that lived in social groups. Ross Barnett at the University of Copenhagen in Denmark and his colleagues focused on Homotherium latidens, sometimes nicknamed the scimitar-toothed cat because its canine teeth were a bit shorter than those in many members of this group of extinct felids. From the proportions of its fossil bones, researchers have long suspected that Homotherium ran after prey rather than waiting in ambush. Barnett and his colleagues discovered evidence in favour of the idea in genetic clues extracted from a Homotherium thigh bone uncovered in Yukon territory, Canada, that is at least 47,000 years old. The cat’s DNA reveals that the ancestors of Homotherium split from other cat groups around 22.5 million years ago. It also includes genes associated with being active during the day, as well as adaptations in the respiratory and circulatory systems related to running. Sabre-toothed cats also have thick, strong front limb bones for grappling prey, says palaeontologist Ashley Reynolds at the University of Toronto, “so it’s very interesting to see positive selection in PGD, a gene associated with bone mineralisation”. Barnett and his colleagues found genes associated with social behaviour, too, hinting that Homotherium may have lived in groups, like lions, rather than living and hunting alone like a leopard. What’s more, the amount of genetic diversity in the sample suggests that Homotherium was much more common than previously thought. “Given the extremely low numbers of Homotherium fossils, this was a shock,” Barnett says. This may mean that many unidentified sabre-toothed cat bones in museum collections really belong to Homotherium. “Skulls and teeth are more readily identifiable than the rest of the body,” Reynolds says.

10-15-20 Exclusive: Concerns raised about vital UK covid-19 infection survey
The UK’s largest scheme for tracking the spread of the coronavirus is at risk of providing a misleading picture of the epidemic, as a growing share of people invited to take part fail to return any test results. The Office for National Statistics’ (ONS) infection survey launched in April to randomly sample thousands of homes in England, and later Wales and Northern Ireland, to estimate how many people are infected with the coronavirus each week. The government’s top scientific advisers consider it the gold standard for measuring the state of the epidemic, because other methods such as testing can miss many cases. When the survey first began, 51 per cent of households invited to take part returned at least one test swab. However, that figure has now dropped to just 5 per cent. The survey’s most recent update, on 9 October, suggested 1 in 240 people in England are currently infected and found a big increase in the incidence rate over the past six weeks, leading to calls for stronger interventions by government. The drop in the response rate has sparked concerns the survey could become biased. If the tests are only being returned by a certain group of people, it may become less reflective of the wider population and the true state of infections. The ONS says it weights the results to avoid this, but this may not work, says Shelia Bird at the University of Cambridge. “Re-weighting may not deal sufficiently with systematic bias.” One example of that bias would be if the small percentage of people returning swabs are also those who are more observant of guidance, and therefore less likely to be exposed to covid-19 – raising the prospect of an underestimate of infections. Paul Hunter at the University of East Anglia says: “The big question is whether or not this drop-out could bias any results and that is a difficult one to answer. In a large study it is certainly possible to adjust the analyses for changing demographics in the remaining cohort by standardising for differences in age, sex and social group.” He says it is not surprising the response rate is dropping, as he found the same during a 2016 infectious disease study.

10-14-20 Where did coronavirus come from? And other covid-19 questions answered
We have now been living with SARS-CoV-2, the virus that causes covid-19, for the best part of a year. In that time, our knowledge has expanded dramatically, but there is still so much we don’t know – and even when we think we know things, the science can change fast. On 24 September, we held a live Q & A event online for subscribers about the pandemic and were inundated with questions. Here, our reporters tackle some of the most common. How does the coronavirus spread through the air? Is aerosol transmission a possibility? The coronavirus definitely infects people via the air. The rather confusing debate among experts is whether it is only carried by large droplets that rapidly sink to the ground or whether people can also be infected by smaller droplets that can remain airborne for hours, known as aerosols. It is very hard to establish exactly how people have been infected, but the overall evidence does suggest that aerosol transmission is happening. To give one example, a study looking at how a passenger on a flight between London and Hanoi in Vietnam infected up to 15 others concluded: “The most likely route of transmission during the flight is aerosol or droplet transmission.” What about aerosols indoors? I’m wondering if I brave a museum visit. The risk is thought to be greatest in crowded, poorly ventilated spaces where people don’t wear masks and shout or sing, such as some pubs. In a spacious museum that isn’t crowded and where everyone is wearing masks, as currently required in the UK, the risk should be lower. However, the risk also depends on the odds of encountering infectious people. If case numbers are rising, these odds rise too. How you travel to the museum will also matter. And how about outdoors? The risk will vary enormously depending on circumstances, such as how windy it is, how many people are around you, how close they are and if any are infectious. Time is also a factor: you might have to stay in close proximity to an infected person for some time to breathe in a high enough dose of the virus to infect you.

10-14-20 'Ums' and 'ers' are a hidden code that helped complex language evolve
Filler words such as uh, mmm and huh may seem inarticulate, but without them human communication would be far less sophisticated. YOU might expect it to take more than a two-letter word to sink a politician’s credibility. But one did just that for Canada’s prime minister, Justin Trudeau, in June 2016. With a huge wildfire burning in the province of Alberta, he had been asked about the country’s capacity to cope. “Uh, certainly, I think we’re, uh, all aware that, uh, uh, a prime minister, uh, showing up at Fort McMurray, when firefighters are busy trying to, uh, uh, contain a massive raging wildfire is, uh, not a particularly helpful thing,” he began. Trudeau went on to use a total of 50 uhs in a statement lasting little more than a minute. A video soon went viral, and online commentators were universally scathing. “Canada’s dumbest, uh, Prime Minister” wrote one viewer. Reading the unedited transcript, you may well have questioned Trudeau’s intelligence yourself. Surely such hesitation is a sign of sloppy thinking and ineloquence. Weren’t we taught as children to eliminate uhs from our conversation? Yet the latest research shows that this is an unfounded prejudice. Far from being an inarticulate waste of breath, filler words like um, uh, mmm and huh are essential for efficient communication, sending important signals about the words we are about to say so that two speakers can better understand each other. “They streamline our interactions, smooth the flow of the conversation and manage our social relations,” says Mark Dingemanse, who studies language and social interaction at Radboud University in the Netherlands. Indeed, he argues that the complexity of our language today couldn’t have emerged without them. To which the obvious response may be, “huh?” It is only recently that scientists have paid filler words any serious attention, with many linguists previously considering them to be mere errors in speech production with no useful function. “People were taught that they were just garbage,” says Jean Fox Tree at the University of California, Santa Cruz. The few studies that were done mainly riffled through that supposed rubbish for clues to deception – with mixed results (see “I’m, uh, telling the truth”).

310-14-20 It is bad science to say covid-19 infections will create herd immunity
AS I write this, my 19-year-old son is self-isolating in his university room with symptoms of covid-19, awaiting test results. He is quite poorly, though overwhelmingly likely to make a full recovery. But I worry that he will be one of the few young adults who get seriously ill or even die, or end up with long-term health problems. To some, however, his illness is welcome; in fact, they wish it on all of his peers. According to the signatories of an open letter called the Great Barrington Declaration, lockdown measures are doing more harm than good and we should open up society and let the virus rip. OK, that is a bit of an exaggeration. The declaration – named after the US town where it was signed – advocates a strategy called “focused protection” under which the most vulnerable people shield and everybody else “should immediately be allowed to resume life as normal”. This will then allow herd immunity to build up. The declaration publicly exposed a scientific disagreement that has been simmering for months. On one side are mainstream scientists who reluctantly see restrictions on freedom as the only way to keep a lid on the pandemic while we wait for vaccines; on the other, the libertarians who see the damage done to economies and individual lives as too high a price. The mainstream media lapped up the disagreement narrative, but completely missed the fundamental problem with the declaration: its extremely dubious claims about herd immunity. This is central to the strategy, but the document badly fluffs the science. Herd immunity is conceptually simple. If enough people become immune to an infectious agent, the entire herd is protected because infectious people rarely encounter a non-immune person, and so transmission fizzles out. The level of individual immunity requited to attain herd immunity depends on how infectious the virus is, as measured by R, the average number of people that each infectious person infects. The classic example is measles, which has an R number of around 15 and a herd immunity threshold of 95 per cent. The numbers for the coronavirus SARS-CoV-2 are about 3.5 and 60 to 70 per cent. Herd immunity has only ever been attained by vaccination. But the declaration advocates naturally acquired immunity. In other words, letting between two-thirds and three-quarters of the population catch the virus.

10-13-20 Covid-19 crisis quashed colds and flus but they may be worse next year
Winter is coming to the north. If what happened in the southern hemisphere is any guide, anti-coronavirus measures could result in fewer people than usual getting flus and colds. The respite may be brief, though. These viruses could come roaring back when measures to limit the spread of covid-19 end. If fewer people susceptible to these viruses are infected this year, there will be more susceptible people around next year, says Daniel Yeoh at Perth Children’s Hospital in Australia. If we fall ill at the moment, we tend to worry that we have covid-19, especially if we have a fever or a cough. But such illness is more likely to be due to cold or flu viruses than to the coronavirus. “Colds and flus still dominate over the coronavirus overall,” says Claire Steves at King’s College London, a member of the team behind the COVID Symptom Study app. The app’s users in the UK, US and Sweden report daily whether they are well or have symptoms. Between 8 and 21 August, for instance, just 0.4 per cent of UK app users who reported symptoms of illness tested positive for the coronavirus, says Steves. People reporting a runny nose and swollen glands were unlikely to test positive, but 90 per cent of those who did have a positive test had severe headaches and fatigue. Another study of key workers in the UK found that only half of the people who thought their symptoms indicated covid-19 actually had the disease. Measures being taken to try to stop the spread of the coronavirus are also making it harder for other respiratory viruses to spread. “The social distancing works for other viruses as well,” says Steves. In some places, the effect has been dramatic. Normally the number of people who go to hospital with an illness diagnosed as flu or respiratory syncytial virus climbs sharply every winter. This winter, in Western Australia, the number of reported cases instead fell to zero most weeks, Yeoh’s team has reported. In fact, Australia, Chile and South Africa have reported just 51 positive results for flu out of 80,000 tests done during the southern hemisphere winter. In the previous three winters, these countries reported 25,000 positive results out of about 180,000 tests.

10-14-20 Some animals may use their penis bone to scoop out a rival's sperm
Complex penis bones capable of removing a rival’s semen could be a way for males to ensure their paternity with a long-term mate. The baculum bone, found in the penis of most male mammals, determines the shape of the penis tip itself and varies widely in form across species, says Charlotte Brassey at Manchester Metropolitan University, UK. Humans are one of a few primate species to have evolved this bone away, while many carnivores have well-developed bones with complex curves and hooks. Brassey’s team used 3D X-ray imaging to compare the bacula of 82 carnivore species, including dogs, wolves, lions, bears, otters, walruses and minks, and concluded that penis bone shape might have a role in what they call “post-copulatory sexual competition”. When females mate with more than one male during the same fertility cycle, the sperm of those males compete to fertilise the few available eggs. The design of the penis tip could displace sperm already present in the reproductive tract, clearing the way for the new male, though it isn’t possible to know without imaging the penis inside the female’s reproductive tract – something the team hopes to do in future. The honey badger’s baculum even looks like an ice cream scoop, says Brassey. “It really seems to just be designed to scoop out other sperm and then cup the cervix.” The team found that the most complex bacula in the study were those of animals generally considered to be socially monogamous, meaning they usually live as a pair for an extended period. Simpler structures – smoother and straighter, like rods – were more commonplace in multiple-mate species which don’t form long-term pairs, like some seals. While it might seem counter-intuitive, many socially monogamous females actually mate outside of their “couple”, meaning the complex penis bone shapes may have evolved as a way for males to ensure their paternity, says Brassey.

10-14-20 Leafcutter ants choose architecturally sound building materials
Ants that construct turrets for their nests choose what to build them with in an architecturally sound way, even when given unfamiliar materials. South American leafcutter ants (Acromyrmex fracticornis) carry plant clippings into underground chambers where they use them to cultivate fungus for food. To promote fungal growth, they build thatch-like turrets that keep rainwater from flooding their nests and that create the correct humidity level. In their natural environment, the ants select thick wooden sticks for the base of the turrets, overlapping them like a log cabin, and lightweight grass for the top, then plaster the interior with clay pellets. The whole process takes three days. “They try to keep [the nest] at about 25°C for the fungus and then really high humidity,” says Daniela Römer at the University of Würzburg, Germany. “Putting plant fibres on top prevents against humidity loss.” To test how the ants choose their building materials, Römer and her colleagues replaced their regular choice of twigs and fresh grass with slivers of processed smooth wood and dry grass. They found that the insects still made the same decisions with these new materials, selecting for thickness at the base and lighter vegetation, which promotes humidity, at the top. This illustrates how relatively simple animals can use social organisation to create complex structures, says Römer. “They just react to what is right in front of them,” she says. “They’re not thinking of what they’re building or how it’s supposed to look. But by organising their behaviour in the whole colony, reacting to each other’s cues and cues from their environment, they actually manage to build very complex structures that you wouldn’t expect such simple animals to be able to do.”

10-13-20 The health benefits of sunlight: Can vitamin D help beat coronavirus?
Been spending a bit too much time indoors? You’re not the only one. Many of us now spend up to 90 per cent of our lives indoors and our retinas are bombarded with artificial light late into the evening. That means compared with our ancestors, we’re exposed to less light during the day and more light at night. This disruption to the light-dark cycle we evolved with is having a profound effect on our circadian rhythms, shifting sleep patterns and affecting our health way more than we might realise. Light levels help to regulate alertness and mood. We also rely on sunlight to convert cholesterol in the skin into vitamin D, which helps build strong bones, and plays a beneficial role in our immune system. Some headlines even suggest that sunlight could and help protect us from the coronavirus. But does the science back that up? And what do we miss when we’re confined indoors? In this week’s Science with Sam, we take a look at the evidence for the health benefits of sunlight, its importance for your mood and some simple tips to maximise your exposure. Before the invention of houses, street lights and Netflix, our ancestors spent most of their days outside, and their nights were illuminated by nothing brighter than firelight. Now we spend 90 per cent of our lives indoors, and our retinas are bombarded with artificial light late into the evening. This affects our sleep, our biology and our health way more than we might realise. The good news is that a little daylight goes a long way. But what does sunlight do for us, and what do we miss when we’re stuck indoors? Our bodies are guided by circadian rhythms, 24-hour cycles in our biology and behaviour that make us feel alert during the day and sleepy at night. These rhythms are regulated by a special set of cells at the back of the eye, behind the rods and cones that enable our brains to construct images. They are called intrinsically photosensitive retinal ganglion cells, or ipRGCs for short. ipRGCs are particularly sensitive to light in the blue part of the spectrum, including bright daylight, and the light from our screens. They send signals to areas of the brain that control alertness. Just one hour of low-intensity blue light can increase reaction speeds as much as drinking two cups of coffee. That’s great if your aim is to be awake, but not so good just before bedtime.

10-13-20 Covid reinfection: Man gets Covid twice and second hit 'more severe'
A man in the United States has caught Covid twice, with the second infection becoming far more dangerous than the first, doctors report. The 25-year-old needed hospital treatment after his lungs could not get enough oxygen into his body. Reinfections remain rare and he has now recovered. But the study in the Lancet Infectious Diseases raises questions about how much immunity can be built up to the virus. The man from Nevada had no known health problems or immune defects that would make him particularly vulnerable to Covid. Scientists say the patient caught coronavirus twice, rather than the original infection becoming dormant and then bouncing back. A comparison of the genetic codes of the virus taken during each bout of symptoms showed they were too distinct to be caused by the same infection. "Our findings signal that a previous infection may not necessarily protect against future infection," said Dr Mark Pandori, from the University of Nevada. "The possibility of reinfections could have significant implications for our understanding of Covid-19 immunity." He said even people who have recovered should continue to follow guidelines around social distancing, face masks and hand washing. Scientists are still grappling with the thorny issue of coronavirus and immunity. Does everyone become immune? Even people with very mild symptoms? How long does any protection last? These are important questions for understanding how the virus will affect us long-term and may have implications for vaccines and ideas such as herd immunity. So far, reinfection seems to be rare - there have been only a few examples out of more than 37 million confirmed cases. Reports in Hong Kong, Belgium and the Netherlands said they were no more serious than the first. One in Ecuador mirrored the US case in being more severe, but did not need hospital treatment.

10-13-20 Implanting beef cattle embryos in dairy cows makes them more lucrative
Farmers in the US have begun implanting dairy cows with fertilised embryos of beef cattle, so they produce calves bred for beef rather than milk production. The idea is to make dairy farming more profitable. Cattle have been bred for either milk or beef production. Beef breeds typically put on more muscle faster for less food than dairy cattle do, and the meat quality is better. This makes beef calves far more valuable than male dairy calves, which are often disposed of immediately after birth. Select Sires in Minnesota has trialled the implantation of beef cattle embryos and is now commercialising the technique. “It’s in its infant stages,” says Chris Sigurdson of Select Sires, but the company hopes the practice will become routine. “That’s the vision.” If it does catch on, it would also help reduce the industry’s substantial greenhouse gas emissions, says Alison Van Eenennaam at the University of California, Davis. “It really alters the sustainability metric.” Dairy cows must keep having calves to maintain milk production. Female dairy calves can be used to replace ageing cows but male dairy calves aren’t nearly as valuable as breeds created specifically for beef production. Some farmers kill male dairy calves after birth, despite efforts to end this practice, because it often costs more to raise them than they can be sold for. In the UK, some of the male dairy calves that are sold are exported to Europe, where there is more demand for veal. This is opposed by welfare organisations because of the long journeys involved. The number of male dairy calves being killed has been reduced by the growing use of reproductive technologies. Many dairy cows are now inseminated with semen from dairy bulls sorted to remove sperm with a Y chromosome. This means the resulting offspring are nearly all female.

10-9-20 Easy interventions like revamping forms help people show up to court
Behavioral “nudges” can prevent people from facing an arrest warrant for a missed court date. Imagine a police officer charging a man with disorderly conduct and issuing a citation for him to appear in court. The man stuffs the slip in his wallet, where it’s soon forgotten. Then, a year later, he’s pulled over for speeding, and learns that his failure to appear in court has resulted in a warrant for his arrest. The man’s situation is surprisingly common. From January 1, 2016 to June 14, 2017, police officers in New York City issued 323,922 criminal summonses for minor infractions, such as being in a closed park after dark, public urination or carrying an open alcohol container outside. Showing up to court frequently results in the case being dismissed. Still, about 40 percent or more of these New Yorkers typically miss their court date, usually scheduled for 60 to 90 days after the citation is issued, resulting in an arrest warrant. But punitive measures like arrests may not be necessary to bring these defendants to court, a new study suggests. Simple interventions, namely revamping the summons form to emphasize the court date and possibility of arrest and sending text reminders for an upcoming court appearance, help reduce no-show rates, researchers report online October 8 in Science. The study evaluated these two policy changes to New York City’s summons process that were gradually phased in during 2016. These “behavioral nudges” resulted in nearly 31,000 fewer arrest warrants from August 2016 to September 2019 than there would have been otherwise, the researchers estimate. These measures will not fix systemic inequities that result in more poor and Black and brown people receiving such summons than others, the authors say, but the changes provide a more humane approach to criminal justice that also saves money. For example, sending every summons recipient three text reminders would cost New York City $4,500 per year, the authors estimate. The approximately 31,000 warrants averted over the three-year period saved an estimated $650,000 from court costs alone.

10-9-20 Stone Age people in Ireland had dark skin and were lactose-intolerant
Some Stone Age people in Ireland left the bodies of their dead to decompose in a natural rocky chamber on a mountain. Genetic analysis of two of these bodies shows they had darker skin, like many people in Europe at the time, and suggests they lived in fairly large communities. The boulder chamber was accidentally discovered in 2016 by a hillwalker exploring Bengorm mountain in north-west Ireland. Finding human bones on the floor, he called the police. The bones turned out to be thousands of years old and the site was turned over to archaeologists led by Marion Dowd at the Institute of Technology Sligo in Ireland. “It’s a Neolithic site that has been completely undisturbed for 4500 to 5000 years,” she says. The team found a total of 4899 bone fragments, which belonged to at least eight individuals, both adults and children. However, the chamber wasn’t these people’s final resting place. Instead, people carried corpses to the chamber and left them there for up to 2 years to allow the flesh to decompose, then took away the skulls and other large bones. “What’s left behind are very small bones and very small fragments,” says Dowd. Such elaborate funerary practices were common in the Neolithic, the last phase of the Stone Age. By this time, the first farmers had moved into western Europe from further east. In the British Isles, they largely replaced the hunter-gatherers that had been living there for millennia. Neolithic funeral practices often lasted years and were probably tied to religious beliefs about the afterlife, says Dowd. “The physical disintegration of the body possibly mirrors the spiritual journey.” Lara Cassidy at Trinity College Dublin in Ireland managed to obtain DNA from two of the bones, belonging to two adult males from around 3000 BC. The pair were distantly related. “We can’t say exactly what that relationship would have been, but it would have been about the same amount of sharing of genetic material as for second cousins,” says Cassidy. “That tells us they’re coming from a community that’s sizeable enough that you can avoid close inbreeding.”

10-8-20 Rotten fish smell sweeter if you have a specific genetic mutation
If you don’t find the smell of fish particularly off-putting, you may have an olfactory gene mutation that makes these odours seem less strong and disagreeable. Kári Stefánsson at Icelandic genomics firm deCODE Genetics and his colleagues have identified a gene, TAAR5, that affects how people perceive odours containing trimethylamine, a compound found in rotten and fermented fish. To study how genetics affects our sense of smell, the researchers asked 9122 Icelandic adults to smell six odours that were presented in pen-like devices. The odours had ingredients found in fish, liquorice, cinnamon, lemon, peppermint and banana. After sniffing each odour, the team asked the participants to name the smell and also rate its intensity and pleasantness on a 7-point scale. The participants also had their genomes sequenced, and the researchers correlated the odour responses with the sequences of olfactory genes. They found three genes of interest, variations of which corresponded to differing smell perceptions. In a separate sample of 2204 people, the team confirmed that two of these genes were linked to increased smell sensitivity and one, TAAR5, was linked to fishy smells specifically. In smell tests, people with a particular variant of TAAR5 were more likely to smell nothing when given the fishy odour, or to describe it with neutral or positive descriptors unrelated to seafood, such as “caramel” or “rose”. The variant affects 2.2 per cent of Icelanders, compared with 0.8 per cent of southern Europeans and 0.2 per cent of Africans. “It seems to be some sort of local selection. In Iceland we have been living on fish mostly for thousands of years,” says Stefansson. “TAAR5 is a very conserved gene, so it’s very similar across species, probably because it has been important to protect us against harmful microorganisms,” says Rosa Gisladottir, also at deCODE. Trimethylamine is also present in bad breath, faeces and blood.

10-8-20 Neandertal babies had stocky chests like their parents
Our evolutionary relatives may have inherited short, deep rib cages from their ancestors. Neandertal babies had chests shaped like short, deep barrels and spines that curved inward more than those of humans, a build that until now was known only for Neandertal adults, researchers say. Neandertals must have inherited those skeletal features rather than developing them as their bodies grew, says a team led by paleobiologist Daniel García-Martínez of the National Research Center on Human Evolution in Burgos, Spain. Stocky, big-brained hominids such as Neandertals needed chest cavities arranged in this way from birth to accommodate lungs large enough to meet their energy needs, the scientists contend October 7 in Science Advances. García-Martínez and his colleagues digitally reconstructed rib cages of four previously excavated, partial Neandertal skeletons from infants and young children. The youngsters are estimated to have died when they were about one to two weeks old, four months or less, 1.5 years and 2.5 years. These finds, dating to between around 40,000 and 70,000 years ago, came from sites in France, Syria and western Russia. Each fossil child had a short, deep rib cage and a short spine behind the ribs relative to human infants. On the most complete specimen — the 1.5-year-old child — the researchers determined that the spine curved sharply into the chest cavity. “The stocky body shape of Neandertals not only passed from parents to children. but also probably passed from ancestral species to their Neandertal descendants,” García-Martínez says. Neandertals, or perhaps their direct ancestors, likely inhabited Europe around 430,000 years ago (SN: 3/14/16). And a Neandertal-like ribcage appeared 1.5 million years ago in an African Homo erectus skeleton, García-Martínez contended in a paper published online July 6 in Nature Ecology & Evolution.

10-7-20 Have we been thinking about covid-19 symptoms all wrong?
HAVE we been getting covid-19 all wrong? As the list of symptoms recognised by health authorities evolves, we are starting to learn that people seem to fall into one of several symptom clusters, and that we might be missing the most important signs of the disease in children. The findings could help researchers better understand how the virus affects individuals differently, and how an outbreak in a preschool might look very different to one in a care home. In January, when the world was first alerted to a new coronavirus spreading in the Chinese city of Wuhan, health authorities listed cough, fever and difficulty breathing as key symptoms. People with severe infections developed pneumonia. The illness looked like many other respiratory infections. With time, that picture evolved and today, both the World Health Organization and the US Centers for Disease Control and Prevention list a plethora of symptoms for covid-19. “Our understanding of the symptoms is changing all the time,” says Angela Rasmussen at Columbia University Mailman School of Public Health. “At the start, we focused on respiratory symptoms because it’s a respiratory disease, but we’ve learned since that it’s much more complex than that.” One of the first discoveries was that the virus seems to trigger more severe symptoms in older people, as well as in those with underlying health conditions. But the effect on any individual can vary hugely – many young people have died, too. “We realised it could be very different from one person to another,” says Carole Sudre at King’s College London. It’s not clear exactly what determines how ill a person might get, but there are plenty of factors that could play a role. “All of these people are from different places, they have different diets, genomes and epigenomes, they have different medical statuses and access to healthcare,” says Rasmussen. “All of those things are going to create a unique environment for the virus to replicate and for unique bodies to respond in different ways.” The way individuals are exposed to the virus could also have an effect, says Rasmussen. Subtly different variants could trigger different immune responses, for example. The amount of virus a person is exposed to might influence which symptoms they develop, too, as could the route of infection, for instance whether by nose, eyes or mouth.

10-7-20 Covid-19 doctor's diary: I hope we got the winter flu vaccine right
LIFE as a general practitioner slowly started returning to normal after the summer. I saw only one patient with “long covid” and none with covid-19 symptoms during September. The local “hot hub” that I helped to set up to deal with people who potentially had covid-19 closed on 28 August amid single-digit cases in the area. Sadly, it wasn’t to last. Last week saw record numbers of daily diagnosed cases in the UK, reaching well in excess of 7000. Restrictions are tightening, and however the government chooses to handle things, many people will become unwell. I am worried. Doctors’ surgeries are likely to get overwhelmed again, and there is no doubt that more patients will be redirected to emergency departments. One of the difficulties facing us as doctors will be assessing people with symptoms also seen in covid-19. Meningitis in children and young people can present with a high temperature and is far more dangerous than covid-19. Many adults – especially those who smoke or have breathing problems – get chest infections in winter, which are also clinically indistinguishable from covid-19. The key to making a correct diagnosis and giving appropriate treatment will be the availability of fast and accurate testing. But currently, children and adults with new covid-19 symptoms have to self-isolate because they can’t access a test, fuelling disruption. It also means vulnerable older people might have to self-isolate and so lose some of the care and company they may receive. Then there is flu, the known unknown. Every year, vaccine manufacturers predict which flu strains to protect against. In a good year, when the actual flu viruses match the vaccine, you are over 40 per cent less likely to get ill from flu if you get the vaccine than someone who hasn’t had it. In recent years, the number of annual UK flu deaths has varied from 4000 to 22,000, and 88 per cent of those who died were over 65. We don’t yet know what flu and covid-19 circulating in the population at the same time will mean. Social distancing and an increase in hygiene awareness may reduce the spread of flu.

10-7-20 Bad balance: why dangerous falls are on the rise around the world
Modern lifestyles are making our balance worse – and leaving us more vulnerable to devastating trips and falls. The good news is, it's never too late to regain your poise. FEW things in life are as embarrassing as falling flat on your face in public. Thankfully, once we have grown out of racing around in parks and playgrounds, it doesn’t happen all that often. Don’t take your grace and poise for granted, though. According to a growing body of research, our ability to balance – one of humanity’s hardest-won evolutionary skills – is beginning to fade away. Around the world, falls that lead to serious injury or death are on the rise, even in the young. And most of the time, the people falling over are sober and doing nothing more complicated than standing or walking. Globally, falls are the second biggest cause of accidental death after traffic accidents. Between 1990 and 2017, the total number of deadly falls around the world nearly doubled. Risk of losing your balance increases with age, so you might think this simply reflects the huge number of baby boomers entering their twilight years. But recent estimates suggest the incidence of falls is rising at a rate that outstrips what would be expected from a growing, ageing population. So what is happening? The decline in our collective stability is prompting scientists to take a closer look at the complex brain-body interactions that underpin our ability to balance, and the ways that it is tied to both cognitive and emotional processing. This system is remarkably complicated, but it turns out that the problems undermining it are relatively simple to pin down. That means there are little things we all can do to improve our balance and reduce the risk of falling. Anyone who has unintentionally hit the deck of late can take comfort in the fact that bipedalism is far from easy – particularly the way people do it, with our torsos balanced precariously over our legs. In fact, this is such a precarious way of getting from A to B that we are the only species on the planet that uses it as our primary mode of transport.

10-7-20 Stimulating the ears and tongue may reduce severity of tinnitus
A device that stimulates the tongue and ears could help reduce the severity of tinnitus, a hearing disorder where people perceive phantom noises such as ringing in their ears. The device, developed by Irish firm Neuromod Devices Limited, includes headphones that play a sequence of tones and white noise into the wearer’s ears, as well as a small mouthpiece that simultaneously provides electrical stimulation to the tongue. “We need more treatment options for tinnitus that can be conveniently used at home but can lead to long-lasting effects,” says Hubert Lim at Neuromod Devices Limited. Around 13 per cent of people in the UK live with persistent tinnitus and about 30 per cent of people will experience it at some point in their lives. Treatments such as cognitive behavioural therapy and counselling are often used to help people manage tinnitus, but there is no cure. Lim and his colleagues tested their device in a trial including 326 people with tinnitus. Over a 12-week period, three groups of participants were asked to use the device twice a day for 30 minutes at a time, with differing patterns of stimulation. The researchers found that treatment with the device significantly reduced the severity of tinnitus symptoms for between 75 and 89 per cent of participants, with improvements persisting up to a year later. “If you make the auditory brain more sensitive to many inputs and acoustic stimuli, then it becomes distracted away and less sensitive or aware of the tinnitus,” says Lim. “This is how we believe the treatment is working.” “The paper makes a huge contribution to the tinnitus literature, not only because it reports a marked benefit for patients who participated in the trial, but because this is the first device trial ever to demonstrate any positive effect and therefore paves the way for further research using this mode of treatment,” says John Phillips at Norfolk and Norwich University Hospital in the UK.

10-7-20 3000-year-old leather balls found in graves may be for ancient sport
The first ball games in Eurasia may have been played 3000 years ago, according to a new analysis of three leather balls unearthed in an ancient cemetery in northern China. One of the men buried with a leather ball also sported the world’s earliest known pair of trousers, which he may have worn while playing. The Yanghai cemetery, which contains more than 500 graves, was in use between about 3200 and 1850 years ago. Archaeologists working there a few years ago uncovered three leather balls from three separate graves. The balls, each about 9 centimetres in diameter, had been stuffed with either leather strips or with wool and hair. Two of them had a red cross painted on one side. According to initial estimates, the leather balls were between 2800 and 2400 years old, making them the earliest known balls in Eurasia. The world’s oldest known ball is 4500 years old and was found in a child’s tomb in Egypt. But now a team of archaeologists, including Patrick Wertmann at the University of Zurich in Switzerland, has carbon-dated the wool stuffing of one ball and concluded it is really between 3130 and 2930 years old. The researchers also carbon-dated artefacts from the graves that yielded the other two balls. They fell within the same range, suggesting all three balls are around 3000 years old. Exactly how the balls were used isn’t clear. The archaeologists who unearthed them also found 10 curved wooden sticks in the cemetery, similar to those used to play polo, a game for horseback riders. The men buried with the balls do seem to have ridden horses, say Wertmann and his colleagues: two had whips in their graves, and the trousers that one of them was wearing had a wide crotch that would make straddling a horse comfortable.

10-7-20 Covid-19 doctor's diary: I hope we got the winter flu vaccine right
LIFE as a general practitioner slowly started returning to normal after the summer. I saw only one patient with “long covid” and none with covid-19 symptoms during September. The local “hot hub” that I helped to set up to deal with people who potentially had covid-19 closed on 28 August amid single-digit cases in the area. Sadly, it wasn’t to last. Last week saw record numbers of daily diagnosed cases in the UK, reaching well in excess of 7000. Restrictions are tightening, and however the government chooses to handle things, many people will become unwell. I am worried. Doctors’ surgeries are likely to get overwhelmed again, and there is no doubt that more patients will be redirected to emergency departments. One of the difficulties facing us as doctors will be assessing people with symptoms also seen in covid-19. Meningitis in children and young people can present with a high temperature and is far more dangerous than covid-19. Many adults – especially those who smoke or have breathing problems – get chest infections in winter, which are also clinically indistinguishable from covid-19. The key to making a correct diagnosis and giving appropriate treatment will be the availability of fast and accurate testing. But currently, children and adults with new covid-19 symptoms have to self-isolate because they can’t access a test, fuelling disruption. It also means vulnerable older people might have to self-isolate and so lose some of the care and company they may receive. Then there is flu, the known unknown. Every year, vaccine manufacturers predict which flu strains to protect against. In a good year, when the actual flu viruses match the vaccine, you are over 40 per cent less likely to get ill from flu if you get the vaccine than someone who hasn’t had it. In recent years, the number of annual UK flu deaths has varied from 4000 to 22,000, and 88 per cent of those who died were over 65. We don’t yet know what flu and covid-19 circulating in the population at the same time will mean. Social distancing and an increase in hygiene awareness may reduce the spread of flu.

10-7-20 Have we been thinking about covid-19 symptoms all wrong?
HAVE we been getting covid-19 all wrong? As the list of symptoms recognised by health authorities evolves, we are starting to learn that people seem to fall into one of several symptom clusters, and that we might be missing the most important signs of the disease in children. The findings could help researchers better understand how the virus affects individuals differently, and how an outbreak in a preschool might look very different to one in a care home. In January, when the world was first alerted to a new coronavirus spreading in the Chinese city of Wuhan, health authorities listed cough, fever and difficulty breathing as key symptoms. People with severe infections developed pneumonia. The illness looked like many other respiratory infections. With time, that picture evolved and today, both the World Health Organization and the US Centers for Disease Control and Prevention list a plethora of symptoms for covid-19. “Our understanding of the symptoms is changing all the time,” says Angela Rasmussen at Columbia University Mailman School of Public Health. “At the start, we focused on respiratory symptoms because it’s a respiratory disease, but we’ve learned since that it’s much more complex than that.” One of the first discoveries was that the virus seems to trigger more severe symptoms in older people, as well as in those with underlying health conditions. But the effect on any individual can vary hugely – many young people have died, too. “We realised it could be very different from one person to another,” says Carole Sudre at King’s College London. It’s not clear exactly what determines how ill a person might get, but there are plenty of factors that could play a role. “All of these people are from different places, they have different diets, genomes and epigenomes, they have different medical statuses and access to healthcare,” says Rasmussen. “All of those things are going to create a unique environment for the virus to replicate and for unique bodies to respond in different ways.”

10-7-20 Nobel prize in chemistry goes to the pioneers of CRISPR gene editing
Emmanuelle Charpentier at the Max Planck Institute for Infection Biology in Germany and Jennifer Doudna at the University of California, Berkeley, have won this year’s Nobel prize in chemistry for pioneering the genome editing tool CRISPR-Cas9. The pair were recognised for their work on the widely used technique, which has applications for new medicines, crops and more. “This is a technology method that can provide humankind with great opportunities,” said Claes Gustafsson of the Nobel Committee for Chemistry, speaking as the prize was announced today at the Royal Swedish Academy of Sciences. “I realised I was very emotional,” said Charpentier, on hearing she had won the prize. Only five women have received the award before. Asked about her view on being part of the first all-female team to win, she said she considered herself a scientist foremost. However, she hoped it would send a “positive message” to young women pursuing a career in science. Charpentier paved the way for CRISPR, which enables scientists to identify a specific piece of DNA in a cell and to edit that DNA, an approach that could be used to prevent disease in humans or make food healthier. As Gustafsson noted, it can be used to fix genetic damage, such as the gene mutation that causes sickle-cell anaemia. The development of CRISPR came when Charpentier was studying the bacterial species Streptococcus pyogenes, which causes numerous illnesses in humans. She identified a molecule known as tracrRNA, a defence mechanism which cleaves the DNA of invading viruses. In 2011, her work was published in the journal Nature, catapulting her to celebrity. That year she met Doudna, an expert in RNA, the molecule similar to DNA that carries information in our cells. Together the scientists recreated the bacterium’s DNA cleaving ability in a lab, which the Nobel committee described as “genetic scissors in a test tube”. Gene editing was possible before their discoveries, but has become much cheaper, faster and more accessible as a result of their work.

10-7-20 Gene-editing tool CRISPR wins the chemistry Nobel
The ‘molecular scissors’ were developed just eight years ago. Turning a bacterial defense mechanism into one of the most powerful tools in genetics has earned Jennifer Doudna and Emmanuelle Charpentier the Nobel Prize in chemistry. The award for these genetic scissors, called CRISPR/Cas 9, is “a fantastic prize,” Pernilla Wittung-Stafshede, a member of the Nobel Committee for Chemistry, said at an Oct. 7 news conference held in Stockholm by the Royal Swedish Academy of Sciences to announce the prize. “The ability to cut the DNA where you want has revolutionized the life sciences. We can now easily edit genomes as desired — something that before was hard, or even impossible.” “The genetic scissors were discovered just eight years ago, but have already benefited humankind greatly,” she said. “Only imagination sets the limits for what this chemical tool … can be used for in the future. Perhaps the dream of curing genetic diseases will come true.” She later amended the statement to say that ethics and law are also important to determine what can and should be done with the tool, as some human gene editing is extremely controversial. Only five other women have ever won the Nobel Prize in chemistry. “I wish that this would provide a positive message specifically to the young … girls who would like to follow the path of science, and I think to show them that women in science can also be awarded prizes, but more importantly that women in science can also have an impact through the research that they are performing,” Charpentier said in response to a question during the news conference. The two will split prize money of 10 million Swedish kronor, about $1.1 million. The tool, a programmable molecular scissors known as CRISPR/Cas9, has been used by bacteria and archaea for millions to billions of years to fight viruses (SN: 4/5/17).

10-7-20 Scientists win historic Nobel chemistry prize for 'genetic scissors'
Two scientists have been awarded the 2020 Nobel Prize in Chemistry for developing the tools to edit DNA. Emmanuelle Charpentier and Jennifer Doudna are the first two women to share the prize, which honours their work on the technology of genome editing. Their discovery, known as Crispr-Cas9 "genetic scissors", is a way of making specific and precise changes to the DNA contained in living cells. They will split the prize money of 10 million krona (£861,200; $1,110,400). Biological chemist Pernilla Wittung-Stafshede, commented: "The ability to cut DNA where you want has revolutionised the life sciences." Not only has the women's technology been transformative for basic research, it could also be used to treat, or even cure, inherited illnesses. Prof Charpentier, from the Max Planck Unit for the Science of Pathogens in Berlin, said it was an emotional moment when she learned about the award. "When it happens, you're very surprised, and you think it's not real. But obviously it's real," she said. On being one of the first two women to share the prize, Prof Charpentier said: "I wish that this will provide a positive message specifically for young girls who would like to follow the path of science... and to show them that women in science can also have an impact with the research they are performing." She continued: "This is not just for women, but we see a clear lack of interest in following a scientific path, which is very worrying." During Prof Charpentier's studies of the bacterium Streptococcus pyogenes, she discovered a previously unknown molecule called tracrRNA. Her work showed that tracrRNA is part of the organism's system of immune defence. This system, known as Crispr-Cas, disarms viruses by cleaving their DNA - like genetic scissors. In 2011, the same year she published this work, Prof Charpentier began a collaboration with Prof Doudna, from the University of California, Berkeley. The two had been introduced by a colleague of Doudna's at a cafe in Puerto Rico, where the scientists were both attending a conference. And it was on the following day, during a walk through the streets of the island's capital, San Juan, that Prof Charpentier proposed the idea of joining forces.

10-7-20 City dwellers are just as helpful as people in towns and villages
Whether you are in a small village or a big city, the likelihood that people will help you seems to depend on the neighbourhood’s relative wealth. A series of tests in neighbourhoods across the UK showed that helpfulness didn’t differ based on whether people live in cities or more rural areas. “There’s no evidence for this idea that city living makes us unfriendly,” says Nichola Raihani at University College London in the UK. From 2014 to 2017, Raihani and her colleague Elena Zwirner, also at University College London, carried out hundreds of tests in 37 different neighbourhoods in cities, towns and villages across the UK, from Abercynon to Glasgow to Wombourne. One experiment involved dropping stamped, addressed envelopes on the ground to see if people picked them up and posted them. In a variant of this, the letters were put on windshields with a note saying: “Could you post this for me please? Thank you.” In another test, Zwirner dropped some cards on the pavement when she was around 5 metres from another pedestrian to see if they would help her pick them up. Sometimes she asked for assistance, while other times she just began picking up the cards. In a third experiment, Zwirner started crossing the road when a car was approaching to see if it would stop. The pair found that people living in less urban neighbourhoods were no more likely to help than those in cities. However, people were much less likely to help if they were in deprived areas, as defined by income and employment in the 2011 UK Census. “You are, on average, about twice as likely to be helped in higher-wealth neighbourhoods,” says Raihani. For instance, in relatively wealthy areas in both cities and towns, around three-quarters of the letters were posted. In poorer neighbourhoods in cities, half were posted. In poorer neighbourhoods in towns or villages, only a third were posted.

10-7-20 Bones from an Iron Age massacre paint a violent picture of prehistoric Europe
Unburied victims and abandoned jewelry suggest a power struggle rather than plunder. Attacked from behind and at times dismembered, the fallen residents of an ancient Iberian village add to evidence that prehistoric Europe was a violent place. Violence in ancient Europe isn’t unheard of, with some unearthed massacres attributed to power struggles after the fall of the Roman Empire around 1,500 years ago (SN: 4/25/18). But a new analysis of bones from 13 victims suggests that a violent massacre occurred at a site in what’s now Spain centuries before the Romans arrived, researchers report October 1 in Antiquity. Finding “partially burnt skeletons and scattered human bones with unhealed injuries caused by sharp weapons demonstrated that this was an extremely violent event,” says archaeologist Javier Ordoño Daubagna of Arkikus, an archaeological research company in Vitoria-Gasteiz, Spain. Ordoño Daubagna and colleagues examined nine adults, two adolescents, a young child and one infant who died sometime between 365 and 195 B.C., in the ancient village of La Hoya. One of the adults was decapitated in a single blow, the team found. And one of the adolescents, a female, had her arm cut off. The researchers found the arm bones nearly three meters away from the girl’s skeleton, with five copper-alloy bracelets still attached. Cracks and flaking of the outer layers of some of the bones suggest that the victims were abandoned after they died, rather than buried, the report shows. Other people may have been trapped inside burning buildings — bone shrinkage and discoloration suggest that the remains were in a fire that reached 350° to 650° Celsius. The fact that the bones were only partially burned suggest that they were not scorched during cremation, a common ritual at the time, the researchers say.

10-7-20 Bird-like dinosaurs that lost a finger show evolution in action
A two-fingered dinosaur may help researchers better understand how animals lose fingers and toes through evolution. Oviraptorids, a group of bird-like dinosaurs that lived in what is now China and Mongolia 100 million years ago, usually had three fingers on each hand. But a set of juvenile skeletons confiscated from fossil poachers at the Mongolia-China border in 2006 have revealed two-fingered hands, suggesting an adaptation. Gregory Funston at the University of Edinburgh in the UK and his colleagues have named the dinosaurs Oksoko avarsan, after a three-headed eagle in Mongolian mythology and the Mongolian word for “rescued”. The dinosaurs had a toothless beak and were probably covered in feathers like other oviraptorids, which share a common ancestor with birds, says Funston, making them resemble a small ostrich. Unlike its three-fingered relatives, the new species had shorter forearms and only two functional, stout fingers with a limited range of motion – a remnant stub of a third finger bone doesn’t emerge from the hand. That means it may have used its hands for nest-building instead of grabbing prey, says Funston. “They might have been moving towards becoming herbivores.” Over millions of generations, animals evolve away body parts that become less useful – including unneeded fingers and toes, says Funston. It is akin to the loss of the tail in humans after they evolved to walk upright. “It requires energy to grow and maintain each structure, so if it’s not needed, the energy is better spent elsewhere,” he says. Funston and his fellow researchers acquired the skeletons after Mongolian customs officials confiscated them from black market fossil traders, he says. While this was enough to confirm the discovery of a new species, the illegal nature of the excavation prevented a full investigation. In particular, the scientists don’t know where the fossil was found, so they can’t study the animals’ environment. “It’s kind of bittersweet,” says Funston.

10-6-20 The search for the origin of life: From panspermia to primordial soup
Did life begin suddenly in a chemical big bang, or did the ingredients come together slowly, bit by bit from a primordial soup? All we know for sure is that life on Earth began sometime between the formation of the planet 4.5 billion years ago and the oldest confirmed fossils 3.4 billion years ago, a window of 1.1 billion years. From Charles Darwin onwards, many scientists have put forward theories about how life got started. Experiments have sought to recreate the conditions of early Earth to see if we can coax simple molecules into something resembling life. Some have even proposed that that life came to Earth from space, a theory called panspermia. This week’s Science with Sam goes in search of our oldest ancestors. Though the answers are still shrouded in mystery, recent findings are taking us closer than ever to the origin of life. In 1953, a graduate student named Stanley Miller mixed four simple chemicals, methane, ammonia, hydrogen and water, in glass tubes, heated them up and shocked them with electricity to mimic lightning. He hoped the experiment would be the key to unlocking the origins of life. But almost 70 years on from the experiment we still don’t have the answer. Figuring it out is going to take some serious detective work. Even the timing is uncertain. All we know for sure is that life began sometime between the formation of Earth 4.5 billion years ago and the oldest confirmed fossils 3.4 billion years ago. That leaves a window of 1.1 billion years. Some people think life could have come to Earth from somewhere else in space, a concept with the slightly off-putting name of panspermia. The idea is that life travelled to earth via a meteoroid or some other kind of space body, from another planet. Somehow surviving the hostile environment of space and the crash landing here on Earth to begin our evolution. But that doesn’t seem very credible since we have no evidence for any life elsewhere in the cosmos, and it doesn’t help us answer the fundamental question of how life arose in the first place. Darwin wondered if life began in a “warm little pond” but the first serious theory about the origin of life was called the primordial soup. Scientists thought w hen Earth was young, the oceans were filled with simple chemicals needed for life, and eventually they assembled themselves into simple living cells. Then came Stanley Miller’s experiment. And while it didn’t create life itself, it did produce amino acids – the building blocks of proteins.

10-6-20 Coronavirus: How to tell which countries are coping best with Covid
As the Covid crisis has unfolded, infection rates have fluctuated and restrictions have proliferated. But it has always felt that there was one idea to cling to: that by working out which countries were doing well - and which were not - there was something to be learned. After all, historians will surely puzzle over how the countries of Western Europe, with broadly similar economies, produced such drastically different outcomes. So far, at least. We use international comparisons all the time, of course - they're a way of measuring how our own governments are doing. But even comparing the simplest data can be complex. There can be differences in how and when death is reported, how co-morbidities are reflected on death certificates, and for how long after a positive test a death is considered to be Covid-related. All will influence how a country's performance at any given moment is measured. For the moment, the gaps in performance appear to be startling. The death rate in Germany stands at around 11.5 deaths per 100,000 people, while in neighbouring Belgium it's more than seven times higher at 87 per 100,000. France stands somewhere in between at around 48 per 100,000 while the UK is nearer the top of the European table, at 63.3 per 100,000. Each is a prosperous country with a capable health-care system and each has applied broadly similar tools to fight the virus, with some combination of lockdowns, social distancing and the encouragement of improved hand hygiene bolstered by localised curfews in some cities. But the further you look into the data the harder it becomes to explain the differences. Lombardia and Veneto for example are neighbouring provinces in Northern Italy, but the differences between their experiences are striking - Lombardia's death rate is 167 per 100,000 and Veneto's 43.

10-6-20 How will Trump’s COVID-19 treatments work together?
In trials, remdesivir, dexamethasone and monoclonal antibodies have individually shown benefits. In the four days since revealing he had COVID-19, President Donald Trump has been treated with three experimental drugs to bring the infection under control: monoclonal antibodies, the antiviral remdesivir and the steroid dexamethasone. Individually, all three treatments have shown promising results in clinical trials. The U.S. Food and Drug Administration has issued emergency use authorization to give remdesivir to patients ill enough to require hospitalization. Several large studies have shown steroids can reduce the risk of death in critically ill patients. And biotechnology company Regeneron Pharmaceuticals just released preliminary antibody results on September 29 from an early-stage clinical trial with 275 COVID-19 patients suggesting a high-dose cocktail of lab-made immune proteins can help speed recovery. But it’s unclear how the drugs might work when used together to treat patients, says Rajesh Gandhi, an infectious diseases physician at Massachusetts General Hospital and Harvard Medical School in Boston. Here’s what we know so far about the treatments used to treat the president. In a news release on October 2, the White House announced that Trump had received a single dose of Regeneron’s antibody cocktail shortly after his diagnosis. (Regeneron, in Tarrytown, N.Y, is a major financial supporter of Society for Science & the Public, which publishes Science News.) That cocktail includes a pair of monoclonal antibodies that each target a different part of the coronavirus’s spike protein. The virus uses the spike protein to pick a cellular lock, called ACE2, to break into cells and begin replicating. By binding to the spike, antibodies can neutralize the virus and curb the infection. Such monoclonal antibodies have been tested early in infection, in people who are not severely ill with COVID-19.

10-6-20 Hepatitis C discoveries win 2020 Nobel Prize in physiology or medicine
Identification of the virus dramatically reduced infections through blood transfusions. Three virologists have won the Nobel Prize in physiology or medicine for the discovery of the hepatitis C virus. Harvey Alter, of the U.S. National Institutes of Health in Bethesda, Md., Michael Houghton, who is now at the University of Alberta in Edmonton, Canada, and Charles Rice, now of The Rockefeller University in New York City, will split the prize of 10 million Swedish kronor, or more than $1.1 million, the Nobel Assembly of the Karolinska Institute announced October 5. About 71 million people worldwide have chronic hepatitis C infections. An estimated 400,000 people die each year of complications from the disease, which include cirrhosis and liver cancer. Today, the major way people get infected is through contaminated needles used for injecting intravenous drugs, but when the researchers made their discoveries in the 1970s, ’80s and ’90s, blood transfusions were an important source of hepatitis C infection. “This is a bit overdue,” says Dennis Brown, chief science officer of the American Physiological Society. It often takes decades before scientific achievements are recognized by the Nobel committee. One reason for the recognition this year may be COVID-19, Brown says. “This keeps virology and viruses in the public eye,” he says. “It might be a push to put science at the forefront, to say when we put money into this and when we have well-funded people working on these viruses, we can actually do something about them.” Alter worked at a large blood bank at NIH in the 1960s when hepatitis B was discovered. (That discovery won the 1976 Nobel Prize in physiology or medicine (SN: 10/23/76).) Blood could be screened so that people wouldn’t get that virus from a transfusion, but patients were still developing hepatitis. Alter and colleagues showed in the mid- and late 1970s that a new virus, dubbed “non-A, non-B” was causing the infection, and that the virus could be used to transmit the disease to chimpanzees (SN: 4/1/78).

10-5-20 Ancient humans harnessed fire to make stone tools 300,000 years ago
Ancient humans used controlled fire to modify their stone tools at least 300,000 years ago. Previously, the oldest hard evidence of controlled fire use was from Pinnacle Point in South Africa, 164,000 years ago. “We just doubled it,” says Filipe Natalio of the Weizmann Institute of Science in Israel. He and his colleagues studied 300,000-year-old flint tools from Qesem cave in Israel. The cave was occupied between 420,000 and 200,000 years ago, and the people who lived there regularly lit fires. Careful heating can change the crystal structure of rocks and make them easier to shape into tools such as blades. However, until now it has rarely been possible to determine which stone tools have been heated. Some bear characteristic fractures, which indicate they were heated, but these don’t always form. “It can also be misleading,” says Mareike Stahlschmidt at the Max Planck Institute for Evolutionary Anthropology in Germany. That is because stones also fracture when they freeze. Natalio’s team has developed a method that uses spectroscopy to examine the atomic structure of stone tools, revealing any alterations caused by heating. “We can see fire where you don’t see it visually,” says Natalio. The team found that many of the stone tools from Qesem cave had been heated. Primitive flakes were heated to over 400°C, but the more advanced blades were heated more gently, to temperatures of around 250°C. These lower temperatures were less likely to shatter the blades when people worked them, but also required more control over the fire. Natalio says the blades probably weren’t placed directly in the fire, which would be too hot, but instead buried in sediment with a fire on top – a trick some people still use to slow-cook large pieces of meat. “Such heat treatment would indicate complex behaviour,” says Stahlschmidt. “People are intentionally changing the properties of a raw material to get what they need.”

10-5-20 What does COVID-19 vaccine efficacy mean?
Predicting how a vaccine will work in the real world is tricky. With several vaccines against COVID-19 in late-phase testing, the business of measuring efficacy is front and center. Determining the efficacy, or how well a vaccine works in a randomized, controlled trial, gives a sense of how much a vaccine could help alleviate the suffering caused by COVID-19. The U.S. Food and Drug Administration recommends vaccines tested against COVID-19 reach an efficacy of 50 percent, at minimum. That means at least a 50 percent reduction in cases of COVID-19 disease in those who are vaccinated compared with those who receive the placebo. Johnson & Johnson, Moderna, Pfizer and AstraZeneca have each begun phase III trials of their vaccines in the United States. These late-phase trials, which will each assess safety and efficacy in tens of thousands of people, randomly assign some participants to receive vaccinations and others a placebo. The companies and the U.S. government, working together as part of Operation Warp Speed, have set a goal of having initial doses of a vaccine available by January 2021 (SN: 7/10/20). It won’t be clear how well any of these vaccines do their job until the companies report full results from those trials; some preliminary results may come out as early as October. The FDA setting a minimum recommendation for efficacy doesn’t mean vaccines couldn’t perform better. The benchmark is also a reminder that COVID-19 vaccine development is in its early days. If the first vaccines made available only meet the minimum, they may be replaced by others that prove to protect more people. But with more than 1 million deaths from COVID-19 worldwide — and U.S. deaths surpassing 200,000 — the urgency in finding a vaccine that safely helps at least some people is at the forefront. “You want to set the bar [for efficacy] high enough so that it is clinically and epidemiologically significant, but low enough that a ‘good enough’ vaccine can be licensed until something better comes along,” says Kawsar Talaat, a vaccine researcher at the Johns Hopkins Bloomberg School of Public Health. The World Health Organization has also set a minimum target of 50 percent efficacy for vaccines tested against COVID-19, but its “preferred efficacy” is at least 70 percent.

10-5-20 Nobel prize for medicine goes to discoverers of the hepatitis C virus
The 2020 Nobel prize in physiology or medicine has been awarded to Harvey Alter, Michael Houghton and Charles Rice for discoveries about the virus that causes hepatitis C virus. The trio’s work led to treatments for the liver-destroying disease. These discoveries have saved millions of lives worldwide and led to the development of drugs that cure 95 per cent of people treated, the Nobel committee said. This could lead to the elimination of the disease. In the 1970s, Alter at the US National Institutes of Health showed that a liver-damaging disease in people given blood transfusions wasn’t due to the hepatitis A or B viruses, and that an unknown infectious agent was responsible. Houghton at Chiron Corporation identified antibodies to the hepatitis C virus, leading to the development of a blood test in 1990. This meant blood contaminated with the virus could be identified, preventing people being infected via blood transfusions. Rice at Rockefeller University in New York developed ways of growing and studying the hepatitis C virus. His work confirmed that the virus was the cause of the disease, and was key to the development of the antiviral drugs now used to treat it. “These developments have saved millions of lives worldwide,” said Gunilla Karlsson Hedestam of the Nobel committee, during a press conference today.

10-5-20 Nobel Prize for Medicine goes to Hepatitis C discovery
Three scientists who discovered the virus Hepatitis C have won the 2020 Nobel Prize in Medicine or Physiology. The winners are British scientist Michael Houghton and US researchers Harvey Alter and Charles Rice. The Nobel Prize committee said their discoveries ultimately "saved millions of lives". The virus is a common cause of liver cancer and a major reason why people need a liver transplant. In the 1960s, there was huge concern that people receiving donated blood were getting chronic hepatitis (liver inflammation) from an unknown, mysterious disease. The Nobel Prize committee said a blood transfusion at the time was like "Russian roulette". Highly sensitive blood tests mean such cases have now been eliminated in many parts of the world, and effective anti-viral drugs have also been developed. "For the first time in history, the disease can now be cured, raising hopes of eradicating Hepatitis C virus from the world," the prize committee said. However, the 70 million people are currently living with the virus, which still kills around 400,000 a year. The viruses Hepatitis A and Hepatitis B had been discovered by the mid-1960s. But Prof Harvey Alter, while studying transfusion patients at the US National Institutes of Health in 1972, showed there was another, mystery, infection at work. Patients were still getting sick after receiving donated blood. He showed that giving blood from infected patients to chimpanzees led to them developing the disease. The mysterious illness became known as "non-A, non-B" hepatitis in and the hunt was now on. Prof Michael Houghton, while at the pharmaceutical firm Chiron, managed to isolated the genetic sequence of the virus in 1989. This showed it was a type of flavivirus and it was named Hepatitis C. And Prof Charles Rice, while at Washington University in St. Louis, applied the finishing touches in 1997. He injected a genetically engineered Hepatitis C virus into the liver of chimpanzees and showed this could lead to hepatitis.

10-5-20 Cannibalism in the womb may have helped megalodon sharks become giants
The ancient sea terror may have grown to 14 meters thanks to a firstborn’s predatory practice. The largest sharks ever to hunt in Earth’s oceans may have gotten so big thanks to their predatory behavior in the womb, scientists report October 5 in Historical Biology. The idea emerged from a study that first analyzed the sizes and shapes of modern and ancient shark teeth, using those data to estimate body sizes of the fish. Paleobiologist Kenshu Shimada of DePaul University in Chicago and colleagues focused on an order of sharks called lamniformes, of which only about 15 species still exist today, including fierce, fast great white and mako sharks as well as filter-feeding basking sharks (SN: 8/2/18). Well over 200 lamniform species existed in the past, some of them quite large, Shimada says. But none is thought to have rivaled Otodus megalodon, commonly called megalodon, which lived between about 23 million and 2.5 million years ago. Determining just how giant these creatures were is challenging, though, because sharks’ skeletons are made of cartilage, not bone, and little remains of now-extinct species but their teeth. However, those teeth are abundant in the fossil record: A single shark can shed tens of thousands of teeth in its lifetime (SN: 8/10/18). Shimada and his colleagues found that the height of megalodon’s tooth crowns was an extreme outlier among their data, suggesting a total body length of at least 14 meters, twice as long as any other shark that isn’t a filter feeder. But four other extinct species of lamniforms exhibited “gigantism,” growing to over six meters long — not megalodon-scale, but still quite large, Shimada says. Gigantism also occurs in several modern species, including great white, mako and thresher sharks.

10-3-20 Neandertal genes in people today may raise risk of severe COVID-19
The same risk factors may protect against other diseases. Some people’s genetic inheritance from Neandertals may raise their risk of developing severe COVID-19. A stretch of DNA on human chromosome 3 was previously found to be associated with an increased risk of developing severe disease from coronavirus infection and of being hospitalized. Some genetic heirlooms passed down after humans interbred with Neandertals more than 50,000 years ago are known to affect immune system function and other aspects of human health even today (SN: 2/11/16). So researchers decided to see whether Neandertals and other extinct human cousins called Denisovans also share the risky region. “I fell off my chair. It was really a surprise to see that the genetic variants were exactly the same as Neandertals’,” says evolutionary geneticist Hugo Zeberg of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, and the Karolinska Institute in Stockholm. Zeberg and his Max Planck colleague Svante Pääbo report the findings September 30 in Nature. About half of people whose ancestors hail from South Asia — particularly Bangladesh — and about 16 percent of people in Europe today carry this bit of Neandertal legacy, the new study finds. The risky DNA was identified as a COVID-19 danger zone in genome-wide association studies, or GWAS, which use statistical methods to find genetic variants that show up more often in people with a particular disease than in those without the disease. In this case, the comparison was between people who have milder forms of COVID-19 and people who required hospitalization. This stretch on chromosome 3 contains multiple genetic variants that are almost always inherited together, forming a block known as a haplotype. Those variants aren’t necessarily the genetic tweaks that lead to more severe disease, but they flag that one or more genes in the region might be responsible for increasing susceptibility to the coronavirus. The researchers are working to figure out which genes in the region might be contributing to susceptibility, Zeberg says.

10-2-20 500-year-old remains may be first African woman to reach the Americas
A 15th-century skeleton buried at the first European settlement in the Americas probably belonged to an unknown African woman, an analysis of her teeth suggests. The woman died in her mid-20s, within about five years of Christopher Columbus’s first voyage to the Americas, and decades before the start of the transatlantic slave trade. “I think it’s possible that she may have been the earliest known individual of African origin to participate in European efforts to establish a settlement in the Americas,” says David Wheat at Michigan State University, who wasn’t involved in the analysis. Columbus first reached the Americas in 1492. The following year, he journeyed there again from Spain in a bid to establish a permanent settlement, ultimately reaching what is now the Dominican Republic and building La Isabela, the first European town in the Americas. Life in La Isabela was tough: during the four years the town was inhabited, the colonists experienced a high mortality rate because of disease and hunger. Many of them ended up in the settlement’s cemetery where, in the 1980s, archaeological investigations unearthed the remains of about 100 people. Now, a team of archaeologists led by T. Douglas Price at the University of Wisconsin–Madison has reanalysed some of the skeletons. They looked at the skeletons of 21 people and measured the proportion of different strontium isotopes in their tooth enamel, which is influenced by the geology of the region in which an individual grew up. Unsurprisingly, 20 of the individuals had a strontium isotopic signature matching that seen in medieval skeletons unearthed in southern Spain. But the final person – a woman who was in her mid-20s when she died – had a distinctive signature. It was more typical of someone who had spent their formative years living in an area where the rocks date back to early Earth – such as in western or central Africa.

10-1-20 Can vitamin D supplements help protect against covid-19?
If newspaper headlines are to be believed, there is a simple way to protect ourselves from the coronavirus: take a daily vitamin D tablet. Some say the benefits are so great that people should take mega-doses. But the scientific evidence doesn’t back up the claims. What should we believe? Vitamin D is a fat-soluble compound made in the skin through the action of sunlight, and is also found in foods such as oily fish. It is chiefly known for building strong bones, but also plays a role in the immune system, including helping to kill virus-infected cells. Some studies had previously suggested that taking vitamin D tablets wards off respiratory infections like coughs and colds, but in June, the UK’s Scientific Advisory Committee on Nutrition (SACN) concluded that the evidence isn’t strong enough to support such an effect. However, it does advise taking a daily supplement for bone health, as do many other health bodies. What about for covid-19? Several researchers have said that vitamin D has potential to protect people from being infected with covid-19, or if they are infected to help to reduce their illness, and some supporting evidence has started to accrue. However, most of the evidence is in the form of observational studies, which can be misleading because they don’t prove that low vitamin D causes infections, just that it correlates with them. For instance, one study to make headlines last week found that people admitted to hospital with covid-19 had half the risk of death if they had adequate vitamin D levels, was of this type. A third factor could be causing both low vitamin D and susceptibility to the virus, for instance obesity, because the vitamin is stored in fat tissue. The best way to assess the benefits of vitamin D supplements would be trials giving people with covid-19 the vitamin to see if it can help treat their symptoms. One recent such study from Spain found that people in hospital with covid-19 who received high doses of vitamin D were much less likely to need intensive care than those who didn’t receive it.

10-1-20 Electronic blood vessels could replace damaged arteries
Electronic blood vessels made from a combination of metal and plastic could be used to replace arteries damaged by cardiovascular disease. Xingyu Jiang at the Southern University of Science and Technology in Shenzhen, China, and his colleagues created their artificial vessel by printing a layer of liquid metal ink, containing gallium and indium, onto a flexible, biodegradble polymer membrane. The liquid metal functions as an electrode. They then rolled up the polymer into a cylinder to create an artificial blood vessel about 2 millimetres wide. The team showed that in a lab setting, sending electrical pulses to the electrode stimulated living endothelial cells – which line the inside of blood vessels – to gather and proliferate on the inside of the artificial vessel. Engineered blood vessels that encourage this process are less likely to result in blood clots, the researchers say. The artificial vessel could also be made more permeable by applying an electrical field to it – a process known as electroporation – allowing it to deliver drugs to neighbouring cells. The researchers were able to use electroporation to deliver a green, fluorescent protein to blood vessel cells surrounding the artificial vessel. To test how well the electronic blood vessels would work in the human body, they were implanted in six New Zealand rabbits, replacing their two carotid arteries, which supply blood to the brain and face. Two rabbits were used as controls. The team monitored the artificial vessels over three months and found that during this time they allowed sufficient blood flow to the brain and face, and didn’t produce an inflammatory response. Using angiography, an x-ray technique that visualises the flow of blood inside vessels, the team found that the artificial vessels functioned as well as natural carotid arteries, with no sign of them narrowing in diameter.

10-1-20 Babies are being fed mother’s poo in effort to boost gut bacteria
Some babies born by Caesarean section in Finland are being given tiny doses of their mothers’ faeces in an attempt to improve their gut bacteria. The team running the study has warned women not to copy the idea on their own, as there can be dangerous microbes in faeces. The doctors conducting the work tested for these microbes, ruling out a third of the mothers from the trial after this screening. “This is not something to do yourself at home,” says Willem de Vos at the University of Helsinki, Finland. “There may be pathogens in the mother’s microbiome.” As knowledge of the bacteria in our gut has grown, there has been increasing interest in trying to change which species are present. Some studies have shown that babies born by C-sections have different gut bacteria than those born vaginally, perhaps because they aren’t as exposed to their mothers’ microbes while they are born. It has been proposed that this is why such children have slightly higher rates of conditions such as allergies, asthma and obesity. Some groups have tried to mimic vaginal birth by wiping the mouths of babies born by C-sections with their mother’s vaginal fluid. While this did make their gut bacteria more like those of vaginally born babies, it didn’t make them identical. That may be because it is their mothers’ faecal bacteria that usually colonises the gut as women often defecate while in labour, and people delivering babies in the past would commonly have had faecal bacteria on their hands, says de Vos. His team recruited 17 women who needed a C-section for medical reasons. Three weeks before the operation, they each gave a stool sample, which was tested for a range of harmful microbes before being frozen. Ten women were ruled out from the study, six of whom because there were signs of harmful microbes in the samples, such as group B streptococci bacteria. For the rest, a few milligrams of their faeces was mixed with some drops of their breast milk and given to the babies in their first feed. After three months, these infants’ gut bacteria were more similar to those of babies born vaginally than those who didn’t have this intervention, according to data from other studies. The team is now conducting a placebo-controlled trial with forty babies. In a larger ongoing study in Sweden, babies are brushed with a gauze that has had contact with a swab put into the mother’s anus.

10-1-20 Chewing sounds are less annoying if you think they come from an animal
People who are annoyed by the sound of chewing are less likely to be vexed if they think it is made by an animal or other non-human source, rather than a person. “I think most people can relate to having some level of aversion to certain sounds,” says Miren Edelstein at the University of California, but people with severe cases are said to have a condition called misophonia. “Individuals with misophonia experience aversion that is so severe and debilitating that it has a major impact on their well-being and quality of life.” Edelstein and her colleagues wanted to find out if it was just the sounds themselves that people find distressing, or if the wider context of a noise can influence how it is perceived. The team looked at 20 self-identified misophonics and a control group of the same number of people, both with an average age of 30. The team first presented all participants with audio clips produced by human chewing and clips that sounded similar, such as an animal chewing or someone walking on gravel. They then repeated these sounds, but this time explained what the participants were hearing – though they sometimes lied. In this second round, the participants were asked to say what they thought was producing the sound. Finally, the team showed the participants the video that went with each audio clip, revealing the full context. In each round, participants were asked to rate how uncomfortable each sound made them feel on a scale from 1 to 10. Those with misophonia found human chewing sounds three times as aversive on average as those without the condition. Misophonics also found human chewing sounds 36 per cent less annoying if they incorrectly believed the noises came from non-human sources, as opposed to when they correctly identified the sounds.

86 Evolution News Articles
for October 2020

Evolution News Articles for September 2020