drivers of SARS-CoV-2 evolution

Have we too quickly proclaimed the end of the SARS-CoV-2 pandemic? While health policies have changed considerably and the much-decried health past seems to have fallen into oblivion, virologists around the world continue to dissect the mechanisms of the evolution of the virus. And if the lines of research are refined, the mystery remains thick around the conditions of emergence of the variants of concern, the risk of which has not been ruled out.

Since the appearance of the virus, a question has animated the thinking of specialists, whether they are studying its genome, the cogs allowing its transmission and its replication in the human body or its system of evolution by comparing it to other viruses, especially the flu. What is the system by which the SARS-CoV-2 virus evolves and what will become of it in the human population which was free of it less than three years ago?

They initially relied on the sequencing of viral genomes in circulation, made possible thanks to unprecedented genomic surveillance. With a reference model in sight, the seasonal influenza virus, which evolves according to a mechanism known as “antigenic shift”. In a virgin and non-immune population, the virus initially encounters no obstacle to its spread but, following vaccination or infection, herd immunity slows it down and the virus gradually evolves.

Highly mutated variants

At least that is what happens with the seasonal influenza virus and directs its evolution in the human population. As the proportion of immunized people increases, the dominant variant against which the immunity is initially directed spreads less quickly, gradually giving the advantage to the viral variants which are less sensitive to it due to slight modifications of the regions of the protein. surface of the virus, following mutations. The virus can thus persist in the population and specialists rely on knowledge of this phenomenon to try to predict the next dominant flu variant.

During the first months of the SARS-CoV-2 pandemic, genomic surveillance revealed a similar phenomenon and virologists began to monitor recurrent mutations affecting the spike protein, such as the mutation at position 484 which seemed to announce adaptation of the virus to population immunity. Until another phenomenon intervenes with this one to foil their predictions, the sudden emergence of highly mutated variants not deriving from the dominant variants.

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