The raging evolutionary war between humans and Covid-19


The race is in. Vaccines against the virus that causes Covid-19 are pricking everyone’s shoulders, the hypodermic spearhead of a year-long scientific triumph. But that protein virus, like all things that infect humans and make them sick, play and dodge.

Virology versus epidemiology. Vaccination versus evolution. Mutation versus mutation, transmission versus infection, virus versus vaccine. Start! You! Engines! Last year (horrible, tragic, not good, very bad) could have seemed like a direct battle between scientists and a virus to find new drugs and vaccines. But this was not just a foot fight; it was also a search for errors, a subtle nudge through a dozen different vectors. Viruses aren’t exactly alive, but they follow the same rulebook as all living things on Earth: adapt or die. Understanding these more hidden forces – how viruses evolve within us, their hosts, and how the ways they pass from person to person change – will define the next phase of the pandemic.

It’s easy to get scared by new variants of the SARS-CoV-2 virus, with its science fiction nomenclature. There’s B.1.1.7, which seems to be a genius at infecting new people. And it has B.1.351 and P.1, perhaps not better at transmitting from one host to another, but better at evading an immune response (a natural one or one induced by a vaccine). A group of those who escape the immune system share the same mutation, even if they are only distantly related. That, as the saying goes, is life. “The way the virus evolves, the fundamentals of evolution, are the same. What is different is that it is developing on a very, very large scale. There are so many infected people and each person has many viruses. So there are many opportunities for the virus to mutate and try new things, “says Adam Lauring, a virologist at the University of Michigan who studies viral evolution. “Every now and then one of those takes off. It’s a rare event, but when the virus has so many opportunities to play with it, it will happen with increasing frequency. ”This is as much an epidemiology game, in other words, as it is evolutionary biology.

So while it may seem that these variants have some kind of evil intent, to make people sicker, to kill all humans! – that’s not what is happening. Viruses want nothing; they are just verbs. Infect, reproduce, infect. A virus that kills too efficiently does not become a virus for long, because dead hosts cannot breathe on non-infected but susceptible suckers. So one hypothesis says that these successful mutations are primarily changes in the way the virus infects. That is, they improve the way the virus enters a human being, or enters a human cell, or reproduces in that cell (because the more viruses a person produces, the more they emit and the more likely it is to reach someone else ).

This is probably why all these similar variants seem to emerge at once and quickly. Viruses are just small amounts of proteins wrapped around large code molecules, of genetic material. In SARS-CoV-2, that material is RNA. And some viruses reveal mutations more often than others.

Viruses evolve because they reproduce (in fact, that’s pretty much their whole trick), and bugs infiltrate that genetic material in the process. Over generations, sometimes those random or “stochastic” errors actually make the virus work better; sometimes they make it worse. That is, the circumstances of the life or the type of life of a virus are contrasted with random changes in the code underlying its genes. (SARS-CoV-2 appears to mutate at roughly the same rate as other RNA viruses, although, like other coronaviruses in its family, it has a built-in error-correcting mechanism. It needs it, because its genome is very large, relatively speaking, three times the size of the genome in HIV, the virus that causes AIDS, for example. “Without proofreading, too many mutations would probably be created per virus replication event to remain viable,” says Katrina Lythgoe, evolutionary epidemiologist Big Data Institute at the University of Oxford. Such a genomic suicide is called crossing the “error catastrophe threshold”).

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