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

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.