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. 2023 Jun:271:127364.
doi: 10.1016/j.micres.2023.127364. Epub 2023 Mar 15.

A systematic review on impact of SARS-CoV-2 infection

Gowripriya Thirumugam  1 , Yashwanth Radhakrishnan  2 , Suresh Ramamurthi  3 , James Prabhanand Bhaskar  4 , Balamurugan Krishnaswamy  5
Affiliations

A systematic review on impact of SARS-CoV-2 infection

Gowripriya Thirumugam et al. Microbiol Res. 2023 Jun.

Abstract

Innumerable pathogens including RNA viruses have catastrophic pandemic propensity, in turn, SARS-CoV-2 infection is highly contagious. Emergence of SARS-CoV-2 variants with high mutation rate additionally codifies infectious ability of virus and arisen clinical imputations to human health. Although, our knowledge of mechanism of virus infection and its impact on host system has been substantially demystified, uncertainties about the emergence of virus are still not fully understood. To date, there are no potentially curative drugs are identified against the viral infection. Even though, drugs are repurposed in the initial period of infection, many are significantly negative in clinical trials. Moreover, the infection is dependent on organ status, co-morbid conditions, variant of virus and geographic region. This review article aims to comprehensively describe the SARS-CoV-2 infection and the impacts in the host cellular system. This review also briefly provides an overview of genome, proteome and metabolome associated risk to infection and the advancement of therapeutics in SARS-CoV-2 infection management.

Keywords: Alternative medicines; Omics; SARS-CoV-2; Variants.

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Conflict of interest statement

Declaration of Competing Interest None.

Figures

Fig. 1
Fig. 1
: The host cell entry mechanism of SARS-CoV-2. RBD of SARS-CoV-2 specifically targets the ACE2 receptor for cell entry. To fuse with the cellular membranes spike protein subunits S1 and S2 has to thole hTMPRSS2 and lysosomal proteases cathepsins mediated proteolytic cleavage which dissociates S1 from S1/S2 boundary and forged structural changes in S2. The SARS-CoV-2 not only quest hACE2, that also targets Neuropilin-1 (NPR-1) The S protein-ACE2 interaction mediated activation of ADAM17 reduced ACE2 expression in the surface thus exacerbates renin-angiotensin system (RAS) imbalance. Higher the S protein-ACE2 interaction directly proportional to ADAM-17 mediated ACE2 shedding which together increases virus internalization.
Fig. 2
Fig. 2
: Timeline of SARS-CoV-2 variant and mutated residues of S protein.
Fig. 3
Fig. 3
: SARS-CoV-2 vaccines development.
See this image and copyright information in PMC

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