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

After a year of isolation, canceled events and virtual meetings, pandemic fatigue is occurring. But even as more people drop their guard and allow security measures to slip, a harvest of rapidly spreading SARS-CoV-2 variants is moving. through populations around the world. The rapid rise of a trio of mutated viruses suggests an increase in transmissibility, which causes viruses to jump from one host to another.

Scientists now compete to decipher exactly how the mixture of mutations of each variant influences viral spread. This research is vital to understanding the risks of current lineages and predicting how future variants could alter the course of the pandemic.

“We have uncontrolled viral spread across much of the world,” says Adam Lauring, an infectious disease physician and virologist at the University of Michigan. “So the virus has a lot of opportunities to evolve.”

More cases mean more deaths and more people suffering lasting impacts due to COVID-19 attacks, but not all news is sad. On the one hand, the latest analyzes of vaccines suggest that they will remain effective against the new variants. And until people get vaccinated, the same measures that are already known to prevent infection, such as masking, distancing, hand washing, ventilation, and spending time outdoors, become even more important in curbing the viral tide. .

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

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

Sometimes, neutral mutations are transmitted by chance and can become common in a population. But changes that are beneficial to the virus can also drive its spread, causing a variant that outperforms other local varieties and can cause cases to grow.

That seems to be what happened in the UK, Brazil and South Africa. In the UK, variant B.1.1.7 probably drove the record rise in COVID-19 cases in the region in January. The variant is now circulating in more than 60 countries, including the United States, and projections suggest it will become the most common virus variety in the United States in mid-March.

An independent emergence lineage called P.1 could also be driving a wave of cases in Manaus, Brazil, where it accounted for nearly half of new COVID-19 infections in December. On Tuesday, Minnesota officials reported the first U.S. case of P.1 in a resident who previously traveled to Brazil. And a third lineage that generates alarms, known as B.1.351, was first detected amid a wave of December infections in South Africa.

But it is not yet known exactly how the mutations gave rise to the variants. A specific mutation, known as N501Y, appeared independently in all three variants, suggesting that it could provide an advantage to the virus. “This is a sign that there is natural selection,” Lauring says.

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

Another possibility is that the new variants will make infected people have more copies of the virus. This translates into a greater viral “spill” of airborne droplets when people talk, sing, cough and breathe. But different studies have produced conflicting results, and the larger study on the subject suggests that new variants are unlikely to increase viral load, says Çevik. The discrepancy may come from the time of the studies, he adds, as previous research suggests that viral loads increase as infections in the community increase.

Mutations can also help spread viruses like SARS-CoV-2 in many other ways. Some could cause sick people to become infected over longer periods of time, for example. Other changes can help viruses survive longer outside the body, or even increase their ability to replicate. And to complicate matters, individual adjustments to the genome of the virus may work differently on their own than as a mosaic of mutations.

Scientists are also baffled by another crucial question: how contagious are the new variants of coronavirus? As evidence of B.1.1.7 movement through the population grows, a recent model suggests that it is 56 percent more transmissible than past forms of the virus, but these numbers are difficult to pinpoint.

Without routine screening, many SARS-CoV-2 infections still glide under the radar, says Ellie Murray, an assistant professor of epidemiology at Boston Health 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 differences in susceptibility between people.

“In general, when you talk about complicated and disordered human beings living their normal life or at least their normal COVID life, it is very difficult to put an exact number to increase transmissibility, especially when you look at this in time. real. Says Angela Rasmussen, a virologist at the Georgetown Center for Global Health Science and Security in Washington, DC

Scientists are less certain of the increased transmissibility of variants that were first seen in Brazil and South Africa. As the P.1 lineage ran through Manaus, more than 70 percent of the local population had already been infected with earlier versions of the virus, which was theoretically high enough to achieve herd immunity. But then the cases increased and it was worried that the variant could bypass the immune defenses of people who had been previously infected.

Similar concerns have been raised about the variant initially found in South Africa, which shares some mutations with P.1. A modeling effort suggests that the propagation of 501Y.V2 could be explained by an increase in transmissibility of around 50 percent. But alternatively, it could be the result of 501Y.V2 evading immunity in 21 percent of previously infected people, and it is possible that both mechanisms work in tandem.

“It’s very hard to know which 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 colleagues used “pseudoviruses” that infect cells with the same proteins as SARS-CoV-2, but are unable to replicate, to study the possibility of the virus dodging our immune systems. . Their results suggest that mutations in 501Y.V2 could decrease the effectiveness of antibodies in the blood of people previously infected with the virus. But understanding whether this can lead to more re-infections or whether it can affect the effectiveness of the vaccine will require further study, she says.

“What we don’t know yet, no one knows, is how much antibody is enough to protect people from infection,” Moore says. “What we need are human clinical trials to really respond if this reduces the effectiveness of the vaccine.”

The increase in variants puts the emphasis on the need for more precautions against the virus, especially as the deployment of vaccines remains slow. Testing, masks, and social distancing will help curb viral spread. And as people get tired of isolation, Çevik stresses that these measures need to be used intelligently, allowing for activity where the risk is low, as outdoors.

In enclosed spaces, including small huts that are now commonly used for outdoor eating, Murray says, the virus is more likely to generate air and infect people with COVID-19. Contact tracking has shown that the risk of viral transmission indoors is 20 times higher than outdoors. While there is still some risk on the outside, it is extremely low for brief contact between people, says Çevik.

“We have to look at the risk on a spectrum,” she says, and think more about when we let the guard down. “I think people care about strangers outdoors, but they forget about everything when they have dinner with their friends.”

Many researchers are also pushing for better facial masks. While not a panacea and should be combined with other measures such as social distancing, masks can help maintain viral spread when people need to enter high-risk areas. Abraar Karan, an internal medicine physician at Brigham and Women’s Hospital at Harvard Medical School in Massachusetts, has advocated a dramatic expansion of the production of high-filtration masks for the general public. “We’re at war with this virus,” he says. “It’s not a joke.”

Experts also stress that government support is key in efforts to stop transmission. People need the resources to isolate safely: places to put them in quarantine and financial support to stay home from work if they are sick. And speeding up vaccinations is vital, as this will slow down the chances of the virus to reproduce and evolve. “The faster we can vaccinate people, the less likely we are to get more out of these variants,” Iwasaki says.

There may be help in the United States as President Joe Biden works to enact his administration’s $ 1.9 trillion plan to fight the pandemic. Still, people will have to work together to stay alert and slow the spread of the virus.

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