Viruses evolve as a result of mutations (mis-incorporations, insertions or deletions and recombination) and natural selection in search of favorable traits, as a replication, more efficient viral transmission and evasion of host defenses. Newly selected traits can be linked in unpredictable ways and raise concerns that the spread and evolution of the virus may lead to increased virulence (severity of the disease). The limited diversity of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) reported during the 2020, attributed to the exonuclease 3-5" test correction function of the non-structural protein 14 (nsp14), led to the view that vaccines based on a single the sequence of viral protein spike (S), that medians the input of the host cell, would probably generate immune protection for all circulating variants ( 1). However, SARS-CoV-2 variants have emerged with S mutations around the world, potential challenges for vaccination and antibody-based therapies. The continued spread of SARS-CoV-2 creates the opportunity to accumulate additional consequential mutations in S and throughout the viral genome.
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