SARS-CoV-2 mutations: the biological trackway towards viral fitness

The outbreak of pneumonia-like respiratory disorder at China and its rapid transmission world-wide resulted in public health emergency, which brought lineage B betacoronaviridae SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) into spotlight. The fairly high mutation rate, frequent recombination and interspecies transmission in betacoronaviridae are largely responsible for their temporal changes in infectivity and virulence. Investigation of global SARS-CoV-2 genotypes revealed considerable mutations in structural, non-structural, accessory proteins as well as untranslated regions. Among the various types of mutations, single-nucleotide substitutions are the predominant ones. In addition, insertion, deletion and frame-shift mutations are also reported, albeit at a lower frequency. Among the structural proteins, spike glycoprotein and nucleocapsid phosphoprotein accumulated a larger number of mutations whereas envelope and membrane proteins are mostly conserved. Spike protein and RNA-dependent RNA polymerase variants, D614G and P323L in combination became dominant world-wide. Divergent genetic variants created serious challenge towards the development of therapeutics and vaccines. This review will consolidate mutations in different SARS-CoV-2 proteins and their implications on viral fitness.

Automated summary

The outbreak of pneumonia-like respiratory disorder in China and its global spread resulted in a public health emergency, putting the SARS-CoV-2 virus in the spotlight. Betacoronaviruses, known for their high mutation rate, recombination, and interspecies transmission, have shown considerable mutations in different proteins, with single-nucleotide substitutions being predominant. Specific mutations in spike glycoprotein and RNA-dependent RNA polymerase have emerged as dominant globally, posing challenges for therapeutics and vaccines.