The race is on. Covid-19 virus vaccines are being shrugged around the world, the tip of the hypodermic spear of a year’s scientific triumph. But that protein virus, like all things that infect people and make them sick, jokes and escapes.
Virology versus epidemiology. Vaccinology versus evolution. Mutation versus mutation, transmission versus infection, virus versus vaccine. Start! Your! Engines! Last year (horrible, tragic, not good at all, very bad) could have seemed like a simple battle between scientists and a virus to find new drugs and vaccines. But this was not just a stand-up fight; it was also a bug hunt – a subtle push on a dozen different vectors. Viruses are not exactly alive, but they continue to have the same registry as any living thing on Earth: they adapt or die. Understanding those more occult forces – how viruses evolve inside us, their hosts and how they change the way they get from one person to another – will define the next phase of the pandemic.
It is easy to be scared about the new variants of the SARS-CoV-2 virus, with their science-fiction nomenclature. There is B.1.1.7, which seems to be a deal for infecting new people. And you have B.1.351 and P.1 – maybe they are not better at transmitting from host to host, but better at avoiding an immune response (a natural one or the kind that a vaccine induces). A lot of those who escape immune share the same mutation, even if they are just related. This, as they say, is life. “The way the virus evolves, the fundamentals of evolution, are the same. What is different is that the game takes place on a very, very large scale. There are so many people who are infected and every person has a lot of viruses. So there are a lot of opportunities for the virus to mutate and try new things, ”says Adam Lauring, a virologist at the University of Michigan who studies viral evolution. “From time to time, one of them takes off. It is a rare event, but when the virus has so many opportunities to play this, it will only happen with an increased frequency. “This is as much a game of epidemiology, in other words, as it is one of evolutionary biology.
So, although it may seem that these variants have a kind of evil intention – to make people sick, to kill all people! – That’s not what happens. Viruses want nothing; they are just verbs. It infects, reproduces, infects. A virus that kills too effectively does not become a virus for a very long time, because dead hosts cannot walk by breathing on uninfected but sensitive suckers. So one hypothesis says that these successful mutations are largely changes in how the virus infects. That is, they improve the way a virus enters a human, or enters a human cell or reproduces in that cell (because the more viruses a person produces, the more they give and the more likely they are to reach a another person).
Probably why all these similar variants seem to appear suddenly and quickly. Viruses are just small pieces of protein wrapped around large molecules of code, genetic material. In SARS-CoV-2, that material is RNA. And some viruses mutate more often than others.
Viruses evolve because they reproduce – in fact, that means almost all of their weight – and mistakes creep into that genetic material in the process. Over the generations, sometimes those random or “stochastic” mistakes actually make the virus better at doing its job; sometimes they make it worse. Which means that the life circumstances or way of life of a virus play against the random changes of the code that underlies its genes. (SARS-CoV-2 appears to move at about the same rate as other RNA viruses, although like other coronaviruses in its family it has a built-in error correction mechanism. It needs it because its genome is so large relatively speaking – three times the size of the HIV genome, the virus that causes AIDS, for example. Oxford University’s Big Data Institute This type of genomic suicide is called crossing the “threshold of error catastrophe.”