The Delta and Omicron Variants of SARS-CoV-2: What We Know So Far

Abstract

The world has not yet completely overcome the fear of the havoc brought by SARS-CoV-2. The virus has undergone several mutations since its initial appearance in China in December 2019. Several variations (i.e., B.1.616.1 (Kappa variant), B.1.617.2 (Delta variant), B.1.617.3, and BA.2.75 (Omicron variant)) have emerged throughout the pandemic, altering the virus's capacity to spread, risk profile, and even symptoms. Humanity faces a serious threat as long as the virus keeps adapting and changing its fundamental function to evade the immune system. The Delta variant has two escape alterations, E484Q and L452R, as well as other mutations; the most notable of these is P681R, which is expected to boost infectivity, whereas the Omicron has about 60 mutations with certain deletions and insertions. The Delta variant is 40-60% more contagious in comparison to the Alpha variant. Additionally, the AY.1 lineage, also known as the "Delta plus" variant, surfaced as a result of a mutation in the Delta variant, which was one of the causes of the life-threatening second wave of coronavirus disease 2019 (COVID-19). Nevertheless, the recent Omicron variants represent a reminder that the COVID-19 epidemic is far from ending. The wave has sparked a fervor of investigation on why the variant initially appeared to propagate so much more rapidly than the other three variants of concerns (VOCs), whether it is more threatening in those other ways, and how its type of mutations, which induce minor changes in its proteins, can wreck trouble. This review sheds light on the pathogenicity, mutations, treatments, and impact on the vaccine efficacy of the Delta and Omicron variants of SARS-CoV-2.

Keywords: Delta plus variant; Delta variant; Omicron variant; SARS-COV-2; vaccination; vaccine efficacy; variant of concern.

Figure 1

Summary of SARS-CoV-2 mutants/variants: (A) illustration of S-protein–ACE2 binding, location of the frequently detected mutations within the spike region of SARS-CoV-2; (B) detailed visualization of mutations that are found within the genomic structure of current VoC lineages (adopted under CC BY 4.0 License from [50]).

Figure 2

Schematic diagrams of the SARS-CoV-2 genome with structure. Reproduction number of wild-type SARS-CoV-2 is 1.1 which is still higher in the emerging variants of SARS-CoV-2. The receptor-binding motif mainly interacts with host receptor for viral host entry (created with Biorender.Com).

Figure 3

Different lineages of SARS-CoV-2 Delta variants (created with Biorender.com).

Figure 4

Structural and receptor-binding characteristics of Omicron subvariants: (a) surface representation of S-trimers of BA.1, BA.2, BA.3, BA.2.13, BA.2.12.1, and BA.4/BA.5 (BA.4/5) variants; (b) structural interpretation and functional verification of the stability of the spike protein of BA.1, BA.2, BA.3, BA.2.13, BA.2.12.1, and BA.4/BA.5 variants. Left, superimposed structures of spike protein and the S2 domains of BA.1 (purple), BA.2 (red), and BA.4/BA.5 (blue). The binding surface areas between S2 subunits of the variants are calculated in the table on the right; (c) thermofluor analysis for these Omicron variants. Analyses were performed as biological duplicates; (d) binding affinities of RBDs of Omicron variants for hACE2 measured by SPR. Analyses were performed as biological duplicates. (Figure 4 is adapted from Yunlong Cao et al. (2022) [89] via CC by 4.0 license.).