Interaction between Sars-CoV-2 structural proteins and host cellular receptors: from basic mechanisms to clinical perspectives

Research output: Chapter in Book/Report/Conference proceedingChapter (peer-reviewed)peer-review

4 Citations (Scopus)

Abstract

Severe acute respiratory syndrome coronavirus 2 (Sars-CoV-2) has caused a global pandemic that has affected the lives of billions of individuals. Sars-CoV-2 primarily infects human cells by binding of the viral spike protein to angiotensin-converting enzyme 2 (ACE2). In addition, novel means of viral entry are currently being investigated, including Neuropillin 1, toll-like receptors (TLRs), cluster of differentiation 147 (CD147), and integrin α5β1. Enriched expression of these proteins across metabolic regulatory organs/tissues, including the circulatory system, liver, pancreas, and intestine contributes to major clinical complications among COVID-19 patients, particularly the development of hypertension, myocardial injury, arrhythmia, acute coronary syndrome and increased coagulation in the circulatory system during and post-infection. Pre-existing metabolic disease, such as cardiovascular disease, obesity, diabetes, and non-alcoholic fatty liver disease, is associated with increased risk of hospitalization, persistent post-infection complications and worse outcomes in patients with COVID-19. This review overviews the biological features of Sars-CoV-2, highlights recent findings that delineate the pathological mechanisms of COVID-19 and the consequent clinical diseases.
Original languageEnglish
Title of host publicationDisorders of protein synthesis
Editors Rossen Donev
PublisherElsevier Inc.
Chapter9
Pages243-277
ISBN (Electronic)9780323997812
ISBN (Print)9780323997805
DOIs
Publication statusPublished - 07 Sept 2022

Publication series

NameAdvances in Protein Chemistry and Structural Biology
Volume132
ISSN (Electronic)1876-1623

Keywords

  • Peptidyl-Dipeptidase A - metabolism
  • Cardiovascular disease
  • Cytokine storm
  • Cardiovascular Diseases
  • NAFLD
  • Sars-CoV-2
  • Hypertension
  • ACE2
  • Humans
  • Diabetes
  • SARS-CoV-2
  • COVID-19

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