Why are some coronavirus variants more infectious?

Abstract

Since the start of the pandemic, SARS-CoV-2 has infected almost 200 million human hosts and is set to encounter and gain entry in many more in the coming months. As the coronavirus flourish, the evolutionary pressure selects those variants that can complete the infection cycle faster and reproduce in large numbers compared to others. This increase in infectivity and transmissibility coupled with the immune response from high viral load may cause moderate to severe disease. Whether this leads to enhanced virulence in the prevalent Alpha and Delta variants is still not clear. This review describes the different types of SARS-CoV-2 variants that are now prevalent, their emergence, the mutations responsible for their growth advantages, and how they affect vaccine efficacy and increase chances of reinfection. Finally, we have also summarized the efforts made to recognize and predict the mutations, which can cause immune escape and track their emergence through impactful genomic surveillance.

Figure 1

Genomic epidemiology of the emerging lineages of SARS-CoV-2: phylogenetic divergence of 3869 strains sequenced between December 2020 and July 2021. Figure created from https://nextstrain.org/ and colored as per clades.

Figure 2

Dominance of the B.1.617.2 (Delta) variant: prevalence of SARS-CoV-2 lineages over time in India. Line plot for seven day average and shaded region corresponding to the 95% CI. Created from https://outbreak.info server.

Figure 3

Mutations in Spike protein S1 subunit have implications in increasing infectivity and reducing vaccine efficacy in COVID-19. Mutations which increase the affinity of the receptor binding domain to the human ACE2 receptor (red) and help escape binding to neutralizing antibody (blue). D614G substitution (orange) stabilizes prefusion conformation and contributes in tighter binding to ACE2. Mutations responsible for increased viral fusion (cyan) by increasing cleavage at the furin cleavage site (yellow). Receptor binding motif at the CTD of the S1 subunit in magenta while all other mutations are depicted in green.