Did we quickly announce the end of the SARS-CoV-2 pandemic? While health policies have changed dramatically and the much-deplored health past appears to have fallen into oblivion, virologists around the world continue to dissect the mechanisms of virus evolution. And if the lines of research are revised, the mystery remains dense about the conditions for the emergence of worrisome variants, the risks of which have not yet been ruled out.
Since the emergence of the virus, a question has arisen in the thinking of specialists, do they study its genome, the gears that allow its transmission and reproduction in the human body or the system of its development by comparing it with other viruses, especially influenza. . What is the system in which SARS-CoV-2 evolves and what will happen in humans who were free of it less than three years ago?
They initially relied on the sequencing of circulating viral genomes, made possible by unprecedented genomic monitoring. With a reference model on the horizon, the seasonal influenza virus, which evolves according to a mechanism known as “antigenic shift”. In virgin and unvaccinated populations, the virus initially has no obstacle to its spread, but after vaccination or infection, herd immunity slows it down and the virus develops gradually.
highly mutated variants
At least that’s what happens with the seasonal influenza virus and directs its evolution in humans. As the proportion of vaccinated people increases, the dominant variant against which immunity is initially directed spreads less rapidly, giving the advantage of less sensitive viral variants due to subtle modifications in the protein regions. Virus, the following mutations. Thus the virus can persist in the population and specialists rely on knowledge of this phenomenon to try to predict the next prevalent type of influenza.
During the early months of the SARS-CoV-2 epidemic, genetic surveillance revealed a similar phenomenon and virologists began to observe recurrent mutations affecting the spike protein, such as the mutation at site 484 that appears to announce the adaptation of the virus to the immune population. Until another phenomenon interferes with this phenomenon to thwart their predictions, the sudden appearance of highly mutated variables does not stem from the dominant variables.
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