Coronavirus: Do Mutations Make You More Infectious?

The coronavirus that is threatening the world right now is not the same as the coronavirus that first emerged in China.

Sars-Cov-2, the official name of the virus that causes Covid-19 disease, and continues to blaze a trail of destruction worldwide, is mutating.

But while scientists have detected thousands of mutations, or changes in the virus’ genetic material, so far it has only been pointed out that one could alter its behavior.

The crucial questions about this mutation are: does this make the virus more infectious, or lethal, in humans? And could it pose a threat to the success of a future vaccine?

This coronavirus is actually changing very slowly compared to a virus-like flu. With relatively low levels of natural immunity in the population, no vaccine, and few effective treatments, there is no pressure to adapt. So far, he’s doing a good job of staying on track as he is.

The remarkable mutation, called D614G and located inside the protein that forms the “spike” of the virus that it uses to penetrate our cells, appeared sometime after the initial outbreak in Wuhan, probably in Italy. It is now seen in up to 97% of samples worldwide.

Evolutionary edge

The question is whether this domain is the mutation that gives the virus any advantage, or is it just by chance.

Viruses don’t have a big plan. They constantly mutate, and while some changes will help a virus reproduce, some may make it difficult. Others are simply neutral. They are a “by-product of the replicating virus,” says Dr. Lucy van Dorp of University College London. They “hitchhike” over the virus without changing their behavior.

The mutation that has emerged could have become widespread only because it occurred early in the outbreak and spread, something known as the “founder effect.” This is what Dr. Van Dorp and her team believe is the likely explanation for the mutation being so common. But this is increasingly controversial.

An increasing number, perhaps the majority, of virologists now believe, as Dr. Thushan de Silva of the University of Sheffield explains, that there is enough data to say that this version of the virus has a “selective advantage,” an evolutionary advantage over The previous version.

Although there is not yet enough evidence to say “it is more transmissible” in people, he says, he is sure that “it is not neutral.”

When studied under laboratory conditions, the mutated virus was better at entering human cells than those without the variation, say Professors Hyeryun Choe and Michael Farzan, at Scripps University in Florida. The changes in the peak protein that the virus uses to attach to human cells appear to allow it to “stick better and function more efficiently.”

But that’s where they drew the line.

Professor Farzan said that the peak proteins of these viruses were different in a way that was “consistent with, but did not demonstrate, increased transmissibility.”

Laboratory results test

At the Genome Technology Center at New York University, Dr. Neville Sanjana, who normally spends his time working on the Crispr gene-editing technology. has gone one step further.

His team edited a virus to have this spike protein alteration and pitted it against a real Sars-CoV-2 virus from the early Wuhan outbreak, without the mutation, in the cells of human tissues. He believes the results demonstrate that the mutated virus is more transmissible than the original version, at least in the laboratory.

Dr. van Dorp notes that “it is unclear” how representative they are of transmission in real patients. But Professor Farzan says these “marked biological differences” were “substantial enough to tip the evidence a little” in favor of the idea that the mutation is making the virus spread better.

Outside of a Petri dish, there is some indirect evidence that this mutation makes the coronavirus more transmissible in humans. Two studies have suggested that patients with this mutated virus have higher amounts of the virus in their swab samples. That might suggest that they were more contagious to others.

However, they found no evidence that those people got sick or stayed in the hospital any longer.

In general, being more transmissible does not mean that a virus is more lethal; in fact, the opposite is usually true. There is no evidence that this coronavirus has mutated to make patients more or less ill.

But even when it comes to transmissibility, viral load is just an indication of how well the virus is spreading within a single person. It does not necessarily explain how good it is to infect others. The research “gold standard”, a controlled trial, has not yet been carried out. That could involve, for example, infecting animals with one or another variant of the virus to see which one spreads the most in a population.

One of the study leaders, Professor Bette Korber of the Los Alamos National Laboratory in the US, said there was no consensus, but the idea that the mutation would increase the viral load in patients “became less controversial as more data accumulated. “

The mutation is the pandemic.

When it comes to looking at the population as a whole, it’s hard to see the virus become more (or less) infectious. Its course has been drastically altered by interventions, including blockages.

But Professor Korber says that the fact that the variant now seems to be dominant everywhere, even in China, indicates that it may have improved in diffusion among people than the original version. Every time the two versions were in circulation at the same time, the new variant took over.

In fact, the D614G variant is so dominant that it is now the pandemic. And it has been for some time, perhaps even since the start of the epidemic in places like the UK and the east coast of the US So while evidence is mounting that this mutation is not neutral, it doesn’t change necessarily how we should think about the virus and its spread.

On a more reassuring note, most developing vaccines are based on a different region of the spike, so this should not have an impact on their development. And there is some evidence that the new form is just as sensitive to antibodies, which can protect you against infection once you’ve had it or been vaccinated against it.

But since the science of Covid-19 is moving so fast, this is something that all scientists, wherever they are on the meaning of current mutations, will be interested in watching.

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