Winter is fast approaching in the Northern Hemisphere, and researchers warn that COVID-19 outbreaks are likely to get worse, especially in regions that don’t have the virus’s spread under control, according to a report in Nature.

“This virus is going to have a heyday,” David Relman, a microbiologist at Stanford University in California, was quoted as saying. “We are looking at some pretty sobering and difficult months ahead.”

Infections caused by many respiratory viruses, including influenza and some coronaviruses, swell in winter and drop in summer. Researchers say it’s too early in the COVID-19 pandemic to say whether SARS-CoV-2 will become a seasonal virus. But growing evidence suggests that a small seasonal effect will probably contribute to bigger outbreaks in winter, on the basis of what is known about how the virus spreads and how people behave in colder months, the world’s leading multidisciplinary science journal said.

People will be interacting more often indoors in places with poor ventilation, which will increase the risk of transmission, according to Mauricio Santillana, a mathematician at Harvard Medical School in Boston, Massachusetts, who models disease spread.

But even if there is a small seasonal effect, the main driver of increased spread will be the vast number of people who are still susceptible to infection, says Rachel Baker, an epidemiologist at Princeton University in New Jersey. That means people in places that are going into summer shouldn’t be complacent either, say researchers.

“By far the biggest factor that will affect the size of an outbreak will be control measures such as social distancing and mask wearing,” says Baker.

Seasonal trends in viral infection are driven by multiple factors, including people’s behaviour and the properties of the virus — some don’t like hot, humid conditions.

Laboratory experiments reveal that SARS-CoV-2 favours cold, dry conditions, particularly out of direct sunlight. For instance, artificial ultraviolet radiation can inactivate SARS-CoV-2 particles on surfaces and in aerosols, especially in temperatures of around 40 °C. Infectious virus also degrades faster on surfaces in warmer and more humid environments3. In winter, people tend to heat their houses to around 20 °C, and the air is dry and not well ventilated, says Dylan Morris, a mathematical biologist at Princeton. “Indoor conditions in the winter are pretty favourable to viral stability.”

To assess whether infections with a particular virus rise and fall with the seasons, researchers typically study its spread in a specific location, multiple times a year, over many years. But without the benefit of time, they have tried to study the seasonal contribution to SARS-CoV-2 transmission by looking at infection rates in various places worldwide.

A study published on October 13 looked at the growth in SARS-CoV-2 infections in the first four months of the pandemic, before most countries introduced controls. It found that infections rose fastest in places with less UV light, and predicted that, without any interventions, cases would dip in summer and peak in winter. In winter, “the risk goes up, but you can still dramatically reduce your risk by good personal behaviour”, says Cory Merow, an ecologist at the University of Connecticut in Storrs, and a co-author of the study. “The weather is a small drop in the pan.”
But Francois Cohen, an environmental economist at the University of Barcelona in Spain, says that testing was also quite limited early in the pandemic, and continues to be unreliable, so it is impossible to determine the effect of weather on the spread of the virus so far.

Baker has tried to tease apart the effect of climate on the seasonal pattern of cases during the course of a pandemic, using data about the humidity sensitivity of another coronavirus. She and her colleagues modelled the rise and fall in infection rates over several years for New York City with and without a climate effect, and with different levels of control measures. They found that a small climate effect can result in substantial outbreaks when the seasons change if control measures are only just managing to contain the virus. “That could be a location where climate might nudge you over,” Baker says. The team posted its results on the preprint server medRxiv on September 10; the authors suggest that stricter control measures might be needed during winter to reduce the risk of outbreaks.

If SARS-CoV-2 can survive better in cold conditions, it’s still difficult to disentangle that contribution from the effect of people’s behaviour, says Kathleen O’Reilly, a mathematical epidemiologist at the London School of Hygiene and Tropical Medicine. “Flu has been around for hundreds of years and the specific mechanism as to why you have peaks of flu in the winter is still poorly understood,” says O’Reilly.

And even if researchers had more reliable data for SARS-CoV-2, they would see only small or negligible seasonal effects so early in the pandemic, when much of the population is still susceptible, says Relman.

Over time, however, seasonal effects could play a more important part in driving infection trends, as more people build up immunity to the virus. This could take up to five years through natural infection, or less if people are vaccinated, says Baker.

But whether a seasonal pattern emerges at all, and what it will look like, will depend on many factors that are yet to be understood, including how long immunity lasts, how long recovery takes and how likely it is that people can be re-infected, says Colin Carlson, a biologist who studies emerging diseases at Georgetown University in Washington DC, the report in Nature concluded.

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A group of researchers have expressed concern about repetitive patterns of data in a paper describing early-phase clinical trials of Russia’s coronavirus vaccine — the first jab worldwide to be approved for widespread use, according to a report in Nature.

In an open letter to the study authors, who published the trial results this month in The Lancet, the researchers highlighted values that seem to be duplicated, and warn that the paper presents its results only as box plots without providing a detailed breakdown of the data on which they are based. “While the research described in this study is potentially significant, the presentation of the data raises several concerns which require access to the original data to fully investigate”, the letter says. It has so far been signed by 38 scientists.

The trials tested two slightly different viral-vector vaccines — which use genetically engineered adenoviruses to produce coronavirus proteins in the body — on 76 volunteers. The results indicated that the vaccine produced a strong immune response, and that side effects were limited to mild, short-term effects, such as irritation at injection sites or headaches, in a few people. In August, the Russian authorities approved the vaccine, called Sputnik V, for widespread use, and have said that it could be available to the general public within months.

This fast-track approval caused consternation among researchers, who argued that the decision to roll out the vaccine before larger safety and efficacy trials had been completed was dangerously rushed.

The open letter was posted on a blog run by molecular biologist Enrico Bucci, who heads a science-integrity company called Resis in Samone, Italy. Bucci says that he noticed irregularities in the Lancet paper soon after it was published.

For example, in one figure in which the authors report their measurements of markers of a type of immune cell in the blood, many members of two groups of nine volunteers tested with different formulations of the vaccine seem to have the same levels. “The odds of this arising by coincidence are extremely small,” Bucci says.

“To see such similar data patterns between unrelated measurements is really not likely,” says Konstantin Andreev, who studies viral respiratory infections at Northwestern University at Evanston, Illinois. “These discrepancies are not minor.” Andreev had been independently concerned about aspects of the clinical trial, and signed the open letter shortly after it was made public.

“We are not alleging scientific misconduct, but asking for clarification about how these apparently similar data points came about,” says Bucci. “When we read reports that Russia had started to inject the vaccine into people outside clinical trials, we felt we had to speak out immediately.” Late-phase clinical trials of the vaccine, which will involve tens of thousands of people, began on August 26.

The paper’s underlying data should be made available, says epidemiologist Michael Favorov, president of DiaPrep Systems, a diagnostics company in Atlanta, Georgia. “We have a lot of questionable data — in terms of its presentation,” he says. “Maybe the data are good — we can’t judge.” He adds that the decision to publish the reports without the underlying data seems unusual. By contrast, when clinical studies involving a coronavirus vaccine that was developed by the pharmaceutical company AstraZeneca and the University of Oxford, UK, were published in the same journal2, they were accompanied by a large amount of supplementary data that other researchers were able to scrutinise.

The Russian paper’s lead author, Denis Logunov at the Gamaleya National Research Centre for Epidemiology and Microbiology in Moscow, did not respond to requests for comment from Nature’s news team. But he told the Russian news outlet Meduza that he did not intend to respond to the open letter. He denied that there were errors in the publication, and stated that measured antibody levels were “exactly as they were presented” in the figures. He added that he was in contact with the Lancet and “was ready to clarify any issues”.

The Lancet declined to comment on its policy for providing data in support of clinical trials that it publishes, but issued a statement saying that it “has invited the authors of the Russian vaccine study to respond to the questions raised in the open letter by Enrico Bucci”, and that it would continue to follow the situation closely, the report said.

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