Abstract

SARS-CoV-2 is a 30,000-nucleotide single-stranded RNA virus encoding structural, non-structural and accessory proteins. Its origin is uncertain, with hypotheses suggesting evolution from bats or pangolins. Genetic recombination events between strains may have resulted in the emergence of SARS-CoV-2, making it capable of infecting humans and increasing its transmissibility. Its mutability rate is similar to that of other coronaviruses, however, due to the occurrence of the pandemic and the propagation clusters, there was an intensification in the number of mutations generated, which evolutionarily gave rise to lineages, sublineages, variants and strains, consecutively. Such mutations, especially non-synonymous ones, phenotypically reflect a variation in virulence, associated with factors of transmissibility, pathogenicity, multiplication, immunological evasion that differ from their ancestors, which are accumulating and becoming fixed in the lineages of this sarbecovirus. In this way, this study aims to understand such non-silent mutations by correlating changes to the viral infectious process.

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