Variants of SARS CoV-2: mutations, transmissibility, virulence, drug resistance, and antibody/vaccine sensitivity

Severe acute respiratory syndrom coronavirus-2 (SARS CoV-2) is the causative agent of coronavirus disease-19 (Covid-19) which has been designated a worldwide pandemic by the World Health Organization on March 11, 2020. Since that time, the virus has mutated and an assortment of variants have been successful at establishing themselves in the human population. This review article describes the SARS CoV-2 genome, hot spot mutations, variants, and then focuses on the Delta variant, finishing up with an update on the Omicron variant. The genome encompasses 11 open reading frames, one of which encodes the spike or S protein that has been the target for vaccines and some of the drugs because of its role in attachment to the human host cell, as well as antibodies. Mutations in the S protein that are common among several of the variants include D614G that increases transmissibility and viral load and is often associated with P323L on the RNA dependent RNA polymerase. N501Y is a mutation in the receptor binding domain of the S protein that increases binding to the ACE-2 receptor on the human host cells by 10 fold. The discussed variants carry combinations of these and other mutations and are classified by the World Health Organization as variants of concern, variants of interest, and variants under monitoring. All variants are characterized by increased transmissibility (relative to the original SARS CoV-2), which is the reason for their ability to establish themselves. Several but not all variants are more resistant to antiviral drugs and less susceptible to antibodies/vaccines. The Delta variant that dominated the world until November 2021 causes an increased risk for hospitalization and death, but is still very susceptible to the current vaccines. The most recent variant, Omicron, is characterized by increased transmissibility and decreased antibody susceptibility.