“Sure, nothing says it can’t happen,” said Jay LeMay, a virologist at the University of Montreal. The fact that the same trait appears in several different populations is also a very pervasive phenomenon in biology, which has its controllable name: evolutionary convergence. For example, the shape and arrangement of the fins are remarkably similar in dolphins and sharks (apart from the caudal fin of course), although the former is a mammal and the latter are fish (in addition to cartilage, and thus is less closely related to mammals than other fish, called “bones” ). Likewise, a large portion of the fauna living in the desert has evolved to sandy color although there is no relationship between them (rodents, lizards, insects, etc.). The ability to digest milk in adulthood has appeared many times throughout history and in unrelated human groups. And so on.
What this means is that when a trait confer an advantage in a specific context or ecosystem, there is a good chance that it will exist in several species. The same principle applies to the COVID-19 variants.
Every time a virus “reproduces” inside a cell, it has to make copies of its genetic material, which always comes with the risk of going wrong. The odds are slim, but as there are still hundreds and hundreds of billions of COVID viruses circulating around the world, these errors (which are considered “mutations”, literally) keep occurring.
Now, genes, as we have already seen in this column, are nothing more or less than protein “prescriptions”, their one and only task is to store information to assemble proteins in the right way. And that’s basically because proteins are sort of volatile molecules, let’s put it that way. They are made like chains whose bonds are other smaller molecules called amino acids, which come in 20 different “types”, and the correct amino acids must be put together in the correct order for the protein to have the correct physical properties. Chemicals to perform their functions.
When a link in the chain is replaced or pulled as a result of a mistake in transcription of the genome, one of two things usually happens: either the mutation has no effect (said to be neutral), or it prevents the protein from folding properly, and the mutation harms the virus – and it will surely be eliminated. By natural selection. Most mutations fall into one of these two “categories.”
But sometimes, the “error” in the gene does something to benefit the virus, giving it an advantage that other viruses do not. “With the number of viruses circulating, the same mutation could certainly appear multiple times, for sure, but will it still be present in the population, and when, that’s another question,” says Mr. LeMay. The mutation could give an advantage, but if it appeared in a person making a trip to the far north when they could not see anyone, there would be no transmission and that strain would die. So there is a matter of chance. “
In the case of the famous “B117″, the variable responsible for the vast majority of infections currently in Quebec, this coincidence wanted to appear and spread first in southern England, before it became dominant in so many. From the planet. This variant features several different mutations, but let’s look at one of them, poetically called N501Y, because it is particularly interesting to our stories of evolutionary convergence. It’s a mutation that alters the “ spiky protein ” that the coronavirus clings to and enters our cells – which is critical to the virus. In the case of COVID, this protein is 1273 amino acids in length, and the 501 link is an amino acid called asparagine (which microbiologists do not refer to with the letter “N”). However, in the Kent variant, there is another amino acid called tyrosine (denoted as “Y”) which is at position 501 – hence the name of the mutation: N501Y. This new “version” of the prickly protein sticks to our cells much better than the old ones, which (along with other mutations) makes this variant even more contagious.
But it is not only in B117 that there is this beneficial mutation. It appeared around the same time (end of 2020) thousands of kilometers from England and in strains very far from B117, i.e. variants P1 (or “Brazilian variant”) and B.1.351 (or “South Africa variant”), what a A recent international study It is explained as a clear example of evolutionary convergence. This article also lists a series of other mutations these three variables have in common. (Note, however, that this is still a “previously published” that has not been peer-reviewed, so it should be viewed with caution even if its authors are serious people.)
And this study isn’t the only one to notice this. At the beginning of last winter, English Public Health Note that another troublesome mutation was circulating in the B117 strain: the E484K mutation, in which the amino acid glutamate (E) is replaced by lysine (K) at position 484 of the spiky protein. This is a mutation that helps the virus attach to our cells as wellIncreased resistance to antibodies It was previously found only in variants P1 and B.1.351. Additionally, British Public Health noted, the E484K mutation appears to have appeared multiple times in the B117 strain.
In short, viruses are constantly changing, and when a mutation is beneficial, they have a good chance of emerging and establishing themselves independently in several different strains. This is what happened all over the world, and Quebec is no exception. A geneticist at the Institute of Public Health, Sandrine Moreira, has sequenced many of the COVID-19 viruses circulating in our region, and assured me that some B117 mutations “appeared” spontaneously in Quebec. She adds, “It is difficult to determine whether a mutation in a different genetic background will have the same effect on the virus, for example a higher susceptibility to transmission. (…) This is of course expected because the virus continues to evolve, but the meaning and effect of that is. [combinaisons de mutations] Specific unknown. “
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