Waves and variants of SARS-CoV-2: understanding the causes and effect of the COVID-19 catastrophe

Abstract

The coronavirus disease-19 has left a permanent mark on the history of the human race. Severe acute respiratory syndrome coronavirus-2 is a positive-sense single-stranded RNA virus, first reported in Wuhan, China, in December 2019 and from there took over the world. Being highly susceptible to mutations, the virus's numerous variants started to appear, and some were more lethal and infectious than the parent. The effectiveness of the vaccine is also affected severely against the new variant. In this study, the infectious mechanism of the coronavirus is explained with a focus on different variants and their respective mutations, which play a critical role in the increased transmissibility, infectivity, and immune escape of the virus. As India has already faced the second wave of the pandemic, the future outlook on the likeliness of a third wave with respect to the Indian variants such as kappa, delta, and Delta Plus is also discussed. This review article aims to reflect the catastrophe of the variants of SARS-CoV-2 and the possibility of developing even more severe variants in the near future.

Keywords: Immune evasion; Mutations; SARS-CoV-2; Vaccines; Variants; Waves.

Fig. 1

Diagrammatic representation of spike glycoprotein showing S1 and S2 domain, where S1 contains NTD and RBD and S2 contains FP, IFP, HR1, and HR2. Polybasic cleavage site at the interface of S1/S2 contains the RRAR amino acid sequence which is the unique feature of SARS-CoV-2

Fig. 2

Diagrammatic representation of trimeric spike glycoprotein attached with two ACE-2 molecules at receptor-binding site (GVEH) in receptor-binding motif in the S1 domain

Fig. 3

Structural representation of spike protein showing major mutations in the Alpha (B.1.1.7) variant: N501Y mutation in the receptor-binding motif-containing receptor-binding site is crucial for binding with the hACE-2 receptor. D614G is the dominant substitution possibly responsible for high infectivity. P681H is important due to its placement next to the furin cleavage site ‘RRAR at S1/S2 junction’. Other important mutations in the spike protein are S982A, A570D, D1118H, and T716I

Fig. 4

Diagrammatic representation of D614G variant: change of Asp (GAU) in D614 to Gly (GGU) amino acid results in the D614G mutation as shown in the green spheres in the trimeric spike protein

Fig. 5

Pictorial presentation showing geographical distribution and phylodynamics of SARS-CoV-2 variants of interest (VOI): Epsilon variant red square B.1.429, pink square B.1.429.1 and green square B.1.427 (A); Eta variant red square B.1.525 (B); Lambda variant red square C.37 (C) [37]

Fig. 6

Schematic representation of spike protein showing various mutations (variants of concern VOC): E484K, N501Y, and K417N mutations in RBD are common in Alpha, Beta, and Gamma variants (a–c). T478K and L452R mutations in RBM of Delta variants (d). Other mutations are highlighted with different color codes

Fig. 7

Pictorial presentation showing geographical distribution and phylodynamics of SARS-CoV-2 variants of concern (VOC): Alpha variant red square B.1.1.7; pink square B.1.274 (A); Beta variant red square B.1.35 (B); Gamma variant red square P.1 (C); Delta variant red square B.1.617.2, pink square AY.1, green square AY.2 (D) [37]