Overview:

Since 2020, the novel coronavirus SARS-CoV-2 has caused respiratory disease (COVID-19) pandemic around the world. The coronavirus spike glycoprotein (S) is a type I transmembrane protein that contains the S1 and S2 subunits and it interacts with the host cell angiotensin-converting enzyme 2 (ACE2) to facilitate viral genome entry (1). The delta variant (B.1.617.2 lineage), first discovered in India, possesses several key mutations that may explain its replacement over the alpha variant. The receptor binding domain (RBD) mutations L452R and T478K lead to increased binding to ACE2 and decreased neutralization potential (2). Mutation D614G increases viral infectivity; mutation P681R in the furin cleavage site promotes the cleavage rate of the S1-S2 making the virus more transmissible and more infectious. As new variants displace the first-wave virus, it is pivotal to evaluate their transmissibility, virulence, and their possible tendency to escape antibody neutralization (3).

Gene Aliases:

2019-nCoV s1, SARS-CoV-2 spike S1, SARS-CoV-2 S1, novel coronavirus spike s1, nCoV spike s1, coronavirus spike S1, Delta variant

Genebank Number:

MN908947

References:

1. Zhou P, et al: A pneumonia outbreak associated with a new coronavirus of probable bat origin. Nature. 2020, 579:270-89.

2. Planas D, et al: Reduced sensitivity of SARS-CoV-2 variant Delta to antibody neutralization. Nature. 2021, 596:276-280.

3. Cherian S, et al: SARS-CoV-2 spike mutations, L452R, T478K, E484Q and P681R, in the second wave of COVID-19 in Maharashtra, India. Microorganisms. 2021, 9, 1542.