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The global pandemic that peaked in 2019 was caused by the SARS-CoV-2 (severe acute respiratory syndrome coronavirus), which had China as its whenua. The whys and wherefores of this outbreak are attributed to the structural competency of the single-stranded RNA virus that continues to evolve posing major health concerns. SARS-CoV-2 with an increased level of genetic mutations alters the characteristics of the virus, such as transmissibility, and antigenicity alongside the development of drug and vaccine resistance. The deeper examination of prominent mutating sites and structures of the virus can give insights into the development of better and more efficient vaccine candidates. This research is steered to delve into the viral dynamics using full genome sequences and decode the genesis behind the structural and functional variances. The genomic data of SARS-CoV-2 variants were obtained from the Global Initiative on Sharing Avian Influenza Data (GISAID), and a set of significant mutations in each of the non-structural proteins (NSPs) 1 through 16 and structural proteins, including envelope, nucleocapsid, membrane, and spike, were identified. The mutations were characterized as stabilizing or destabilizing and their significance was analyzed with respect to self and in the context of interacting partners. Among all the proteins, NSP6 stands out as a dark horse with extremely high mutability. The results augment our understanding of how mutational events influence virus pathogenicity and evolution. |
