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1.
Protein J ; 41(4-5): 444-456, 2022 10.
Artigo em Inglês | MEDLINE | ID: mdl-35913554

RESUMO

Using molecular dynamics simulations, the protein-protein interactions of the receptor-binding domain of the wild-type and seven variants of the severe acute respiratory syndrome coronavirus 2 spike protein and the peptidase domain of human angiotensin-converting enzyme 2 were investigated. These variants are alpha, beta, gamma, delta, eta, kappa, and omicron. Using 100 ns simulation data, the residue interaction networks at the protein-protein interface were identified. Also, the impact of mutations on essential protein dynamics, backbone flexibility, and interaction energy of the simulated protein-protein complexes were studied. The protein-protein interface for the wild-type, delta, and omicron variants contained several stronger interactions, while the alpha, beta, gamma, eta, and kappa variants exhibited an opposite scenario as evident from the analysis of the inter-residue interaction distances and pair-wise interaction energies. The study reveals that two distinct residue networks at the central and right contact regions forge stronger binding affinity between the protein partners. The study provides a molecular-level insight into how enhanced transmissibility and infectivity by delta and omicron variants are most likely tied to a handful of interacting residues at the binding interface, which could potentially be utilized for future antibody constructs and structure-based antiviral drug design.


Assuntos
Evolução Molecular , SARS-CoV-2 , Enzima de Conversão de Angiotensina 2/química , Humanos , Simulação de Dinâmica Molecular , Mutação , Ligação Proteica , Mapeamento de Interação de Proteínas , SARS-CoV-2/genética , Glicoproteína da Espícula de Coronavírus/química
2.
Protein Sci ; 30(11): 2206-2220, 2021 11.
Artigo em Inglês | MEDLINE | ID: mdl-34558135

RESUMO

Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) is a pathogenic coronavirus causing COVID-19 infection. The interaction between the SARS-CoV-2 spike protein and the human receptor angiotensin-converting enzyme 2, both of which contain several cysteine residues, is impacted by the disulfide-thiol balance in the host cell. The host cell redox status is affected by oxidative stress due to the imbalance between the reactive oxygen/nitrogen species and antioxidants. Recent studies have shown that Vitamin D supplementation could reduce oxidative stress. It has also been proposed that vitamin D at physiological concentration has preventive effects on many viral infections, including COVID-19. However, the molecular-level picture of the interplay of vitamin D deficiency, oxidative stress, and the severity of COVID-19 has remained unclear. Herein, we present a thorough review focusing on the possible molecular mechanism by which vitamin D could alter host cell redox status and block viral entry, thereby preventing COVID-19 infection or reducing the severity of the disease.


Assuntos
COVID-19 , Estresse Oxidativo/efeitos dos fármacos , SARS-CoV-2/metabolismo , Índice de Gravidade de Doença , Internalização do Vírus/efeitos dos fármacos , Vitamina D/uso terapêutico , Enzima de Conversão de Angiotensina 2/metabolismo , COVID-19/metabolismo , COVID-19/patologia , COVID-19/prevenção & controle , Humanos , Espécies Reativas de Nitrogênio/metabolismo , Espécies Reativas de Oxigênio/metabolismo
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