Affiliation:
1. Pharmidex Pharmaceutical Ltd., London, United Kingdom
2. Cellular and Molecular Research Centre, Iran University of Medical
Sciences, Tehran, Iran
3. Nanotechnology and Regenerative Medicine Commercialization Centre (NanoRegMed Ltd), London
BioScience Innovation Centre, 2 Royal College Street, London, United Kingdom
Abstract
Abstract:
In 2019, the whole world came together to confront a life-threatening virus named SARS-CoV-2,
causing COVID-19 illness. The virus infected the human host by attaching to the ACE2 and CD147 receptors
in some human cells, resulting in cytokine storm and death. The new variants of the virus that caused concern
are Alpha, Beta, Gamma, Delta, and Epsilon, according to the WHO label. However, Pango lineages designated
them as B.1.1.7, B.1.351, P.1, B.1.617.2, and B.1.429. Variants may be progressively formed in one chronic
COVID-19 patient and transmitted to others. They show some differences in cellular and molecular mechanisms.
Mutations in the receptor-binding domain (RBD) and N-terminal domain (NTD) lead to alterations in
the host's physiological responses. They show significantly higher transmissibility rates and viral load while
evading neutralizing antibodies at different rates. These effects are through mutations, deletion, and conformational
alterations in the virus, resulting in the enhanced affinity of RBD to PD of ACE2 protein, virus entry, and
spike conformational change. In the clinical laboratory, new variants may diagnose from other variants using
specific primers for RBD or NTD. There are some controversial findings regarding the efficacy of the developed
vaccines against the new variants. This research aimed to discuss the cellular and molecular mechanisms
beyond COVID-19 pathogenesis, focusing on the new variants. We glanced at why the mutations and the ability
to transmit the virus increase and how likely the available vaccines will be effective against these variants.
Publisher
Bentham Science Publishers Ltd.
Subject
Drug Discovery,Pharmacology
Cited by
1 articles.
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