The Proofreading function and mutations in SARS-CoV-2 and their impact on viral infectivity
DOI:
https://doi.org/10.58445/rars.123Keywords:
SARS-CoV-2, Mutation, Proofreading function, Spike protein, Viral infectivityAbstract
SARS-CoV-2 is a positive-sense single-stranded RNA virus that causes the respiratory disease, COVID-19 (coronavirus disease 19) and is a member of the severe acute respiratory syndrome-related coronavirus species in the Coronaviridae family. The virus has led to more than 590 million infections and more than 6.4 million deaths worldwide as of the end of August 2022. The coronavirus family also includes SARS-CoV, which is the virus that led to the 2003 SARS epidemic, affecting 26 countries at the time. Mutations in SARS-CoV-2 have accumulated since the emergence of the virus in 2019, and new variants are increasingly observed. SARS-CoV-2 has a unique proofreading function that has been shown to be carried out by a protein complex that corrects mismatched base pairs during replication. This paper aims to address the degree that the SARS-CoV-2’s proofreading mechanism results in fewer protein mutations in its spike glycoprotein compared to other viruses. The proofreading function limits the number of mutations that survive RNA replication for the SARS-CoV-2 virus. Examining the proofreading function of the SARS-CoV-2 virus will reveal important insights into its mutation rates and changes in viral infectivity, suggesting pathways for treatments in the future.
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