Why some coronavirus variants are more contagious and how we can stop them

After a year of isolation, canceled events and virtual meetings, pandemic fatigue sets in. But even as more people let their guard down and let security measures slip by, a crop of rapidly spreading variants of SARS-CoV-2 is moving through populations around the world. The rapid rise of a trio of mutated viruses suggests an increase in transmissibility, speeding up virus jumps from one host to another.

Scientists are now rushing to decipher exactly how the jumble of mutations in each variant influences viral spread. This research is essential for understanding the risks of current lineages and predicting how future variants might alter the course of the pandemic.

“We have an uncontrolled viral spread over much of the world,” says Adam Lauring, infectious disease physician and virologist at the University of Michigan. “The virus therefore has many opportunities to evolve.”

More cases mean more deaths and more people suffering the lasting impacts of COVID-19 episodes – but not all the news is gloomy and dire. On the one hand, the latest analyzes of the vaccines suggest that they remain effective against the new variants. And until people are vaccinated, the same measures already known to prevent infection – such as masking, keeping away, hand washing, ventilating, and time being outdoors – become even more important. to stem the viral tide.

“The variants may be more transmissible, but the physics haven’t changed,” says Müge Çevik, an infectious disease physician at the University of St. Andrews in Scotland.

A virus replicates by hijacking the cellular machinery of its host to make copies of itself. But like a person who makes mistakes by typing the same sentence over and over again, genetic copies accumulate small mistakes, or mutations. Many changes do not affect the function of the virus, and some even interfere with the ability of SARS-CoV-2 to multiply, but they continue to occur. “Viruses mutate; that’s what they do, ”says Akiko Iwasaki, an immunologist at the Yale School of Medicine in Connecticut.

Sometimes neutral mutations are passed on by chance and can become common in a population. But changes that are beneficial to the virus can also cause it to spread, leading to a variant that outperforms other local varieties and may lead to an increase in cases.

This seems to be what happened in the UK, Brazil and South Africa. In the UK, variant B.1.1.7 likely caused the region’s record peak of COVID-19 cases in January. The variant is now circulating in more than 60 countries, including the United States – and projections suggest it will become the most prevalent variety of virus in the United States by mid-March.

An independent line called P.1 could also be behind a spate of cases in Manaus, Brazil, where it accounted for nearly half of new COVID-19 infections in December. On Tuesday, Minnesotan officials reported the first US case of P.1 in a resident who had previously traveled to Brazil. And a third alarming bloodline, known as B.1.351, was first spotted amid a December spate of infections in South Africa.

But exactly how the mutations gave the variants a head start remains unclear. A specific mutation, known as N501Y, appeared independently in all three variants, suggesting that it could provide an advantage to the virus. “It’s a sign that there’s natural selection going on,” Lauring says.

The N501Y mutation affects the virus spike protein, which is the key it uses to unlock entry into its host’s cells. Laboratory experiments suggest that this mutation improves the ability of the spike protein to bind to cells, suggesting that it may increase the ability of variants to infect hosts.

Another possibility is that the new variants will cause infected people to harbor more copies of the virus. This results in a greater viral “shedding” of airborne droplets when people talk, sing, cough and breathe. But different studies have produced conflicting results, and the largest study on the subject suggests that the newer variants should not increase viral load, Çevik says. The discrepancy may stem from the timing of the studies, she adds, as previous research suggests that the viral load increases as infections in the community increase.

Mutations can also help viruses such as SARS-CoV-2 spread in many other ways. Some can make patients contagious for longer periods, for example. Other changes could help viruses survive longer outside the body, or even increase their ability to replicate. And to complicate matters, individual changes to the virus’s genome may work differently on their own than they do as a patchwork of mutations.

Scientists are also wondering about another crucial question: just how much more contagious are the newer variants of the coronavirus? As evidence for the movement of B.1.1.7 across the population increases, a recent model suggests that it is 56 percent more transmissible than past forms of the virus – but these are hard numbers to pin down.

Without routine screening, many SARS-CoV-2 infections still go under the radar, says Ellie Murray, assistant professor of epidemiology at the Boston University School of Public Health in Massachusetts. This makes it difficult to get an accurate picture of what is going on. Our own human complexities also present a challenge, such as the differences in susceptibility between people.

“Overall, when you talk about complicated, messy humans leading their normal lives – or at least their normal COVID lives – it’s really hard to put an exact number on the increase in transmissibility, especially when you watch this in real time, ”says Angela Rasmussen, virologist at the Georgetown Center for Global Health Science and Security in Washington, DC

Scientists are less certain of the increased transmissibility of variants first spotted in Brazil and South Africa. As the P.1 line roamed Manaus, more than 70% of the local population had already been infected with previous versions of the virus, which was theoretically high enough to achieve herd immunity. But then the cases increased, raising concerns that the variant could bypass the immune defenses of people who had already been infected.

Similar concerns have been raised regarding the variant originally found in South Africa, which shares some mutations with P.1. A modeling effort suggests that the spread of 501Y.V2 could be explained by an increase in transmissibility of about 50 percent. But it could also be the result of 501Y.V2 evading immunity in 21% of people previously infected – and it’s possible that the two mechanisms work in tandem.

“It’s really hard to know which one is which,” says Penny Moore, a virologist at the National Institute of Communicable Diseases and the University of the Witwatersrand in South Africa.

Moore and his colleagues have used “pseudoviruses” that infect cells using the same proteins as SARS-CoV-2, but which are not able to replicate, to study the possibility that the virus is avoiding our immune system. His results suggest that mutations in 501Y.V2 may decrease the effectiveness of antibodies in the blood of people previously infected with the virus. But understanding whether this could lead to more re-infections or if it could affect the effectiveness of the vaccine will require further study, she says.

“What we don’t know yet – nobody knows – is how much antibody is enough to be able to protect people from infection,” says Moore. “What we need are clinical trials in humans to really see if it reduces the effectiveness of the vaccine.”

The rise of variants underscores the need to take more precautions against the virus, especially as vaccine deployment remains slow. Testing, masks and social distancing will all help stem the spread of the virus. And as people tire of isolation, Çevik stresses that these measures need to be used intelligently, allowing activities where risk is low, like outside.

In confined spaces – including small hutches now commonly used for outdoor dining, Murray says – the virus is more likely to grow in the air and infect people with COVID-19. Contact tracing has shown that the risk of viral transmission indoors is 20 times greater than outdoors. While some risk is always present outdoors, it is extremely low for brief contact between people, Çevik says.

“We have to look at risk in a spectrum,” she says, and think more as we let our guard down. “I think people worry about strangers in the open air, but they forget everything when they have dinner with their friends.”

Many researchers are also pushing for better masks. While not a panacea and should always be combined with other measures such as social distancing, masks can help stem the spread of the virus when people must enter high-risk areas. Abraar Karan, an internal medicine doctor at Brigham and Women’s Hospital at Harvard Medical School in Massachusetts, has advocated dramatically increasing production of high-filtration masks for the general public. “We are at war with this virus,” he said. “This is not a joke.”

Experts also point out that government support is essential in efforts to stop transmission. People need the resources to safely isolate themselves – places of quarantine and financial support to stay home from work when sick. And speeding up vaccinations is vital, as it will reduce the opportunities for the virus to replicate and evolve. “The faster we can get people vaccinated, the less likely it is that more of these variants will appear,” says Iwasaki.

Aid may be underway in the United States as President Joe Biden struggles to implement his administration’s $ 1.9 trillion plan to fight the pandemic. Even so, people will need to work together to stay vigilant and slow the spread of the virus.

“It’s not forever; it’s not even necessarily the next six months, ”says Rasmussen. But “right now, the immediate future is not the time to relax.”