Cross Talk on SARS-CoV-2 and Human Immunity

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus that causes coronavirus disease 2019 (COVID-19) is now the leading cause of death globally. This review elaborated the human immune response to SARSCoV-2 and its immune evasion mechanisms as well as factors that determine the case fatality rate and effective immunity using articles selected from PubMed, Medline, Google Scholar and Science Direct that provided an in-depth knowledge of the immunopathogenesis of SARS-CoV-2. Findings from the forty eligible reviewed articles revealed that the host-viral interaction to SARS-CoV-2 involves the recognition of SARS-CoV-2, recruitment of adaptor proteins and antigen presentation which activates both innate and adaptive immunity involved in inhibition of viral replication (interferons), destruction of virus-infected cells (natural killer cells and CD8 cells) and viral clearance. However, SARS-CoV-2 subverts human immunity using multiple strategies such as production of double membrane vesicles, repression of adaptor proteins, interferons and antigen presentation. Accumulating shreds of evidence have shown that several factors such as age, sex, comorbidities, obesity, and lifestyle factors affect immune responsiveness to SARS-CoV-2. Hence, better knowledge of the viral interactions with the host and factors determining prevalence and severity is fundamental to the management and development of effective and biocompatible prophylactic and therapeutic options.

The Impacts of Anti-Inflammatory Agents on COVID-19 Cytokine Storm

“…The entrance of SARS-CoV-2 occurs mainly into alveolar epithelial cells, vascular endothelial cells, airway epithelial cells, and macrophages that express a high level of angiotensin converting enzyme 2 (ACE2) receptor [6]. The virus's adhesion, fusion, and entry are mediated by proteases such as transmembrane serine protease, AP2-associated protein kinase, and cathepsin [7].…”

“…The virus's adhesion, fusion, and entry are mediated by proteases such as transmembrane serine protease, AP2-associated protein kinase, and cathepsin [7]. Once inside the infected cell, the viral genomic singlestranded RNA or other RNA compositions (double-stranded RNA) are recognized by a network of receptors called pathogen-recognition receptors (PRRs) such as Toll-like receptors (TLRs) and cytoplasmic retinoic acid-inducible gene 1 (RIG-1)-like receptors (RLRs) [6]. As part of innate immunity against SARS-CoV-2, recognition of the virus by PRRs leads to the activation of adaptor proteins (activator protein-1 (AP-1), interferon regulatory factor 3 (IRF3), and nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB)), which induces intracellular signaling responsible for both transcriptional and posttranscriptional production of interferons (IFNs), the key agent for antiviral immunity.…”

“…IFNs use dependent and independent mechanisms of class 1 major histocompatibility complex (MIC) proteins to stimulate natural killer (NK) cells involved in immunomodulatory and anti-inflammatory activities [8]. Regrettably, the protective role of IFNs in viral clearance is abrogated by SARS-CoV-2 via different immune evasion mechanisms that not only impair viral clearance but also promote paradoxical hyperinflammatory cytokines [6].…”