Title:An Updated Review on Complicated Mechanisms of COVID-19 Pathogenesis
and Therapy: Direct Viral Damage, Renin-angiotensin System
Dysregulation, Immune System Derangements, and Endothelial Dysfunction
Volume: 22
Issue: 7
Author(s): Shahab Falahi, Maryam Maleki and Azra Kenarkoohi*
Affiliation:
- Zoonotic Diseases Research Center, Ilam University of Medical Sciences, Ilam, Iran
- Department of Microbiology, Faculty of Medicine,
Ilam University of Medical Sciences, Ilam, Iran
Keywords:
SARS-CoV-2, COVID-19, pathogenesis, Renin-angiotensin system, thromboinflammation, immunopathogenesis.
Abstract: SARS-CoV-2 was reported as the cause of coronavirus disease 2019 (COVID-19) in late
December 2019. According to sequencing and phylogenetic studies, the new virus belongs to Coronaviridae
family and Betacoronavirus genus. Genomic sequence analysis has shown SARS-CoV-2 to
be similar to SARS. SARS-CoV-2 is more infectious, and the high level of COVID-19 community
transmission has led to a growing pandemic. Although infections in most patients with COVID-19 are
moderate or mild, 20% of the patients develop a severe or critical form of the disease. COVID-19 may
affect a wide range of organs and tissues, including the respiratory system, digestive system, nervous
system, and skin. Patients with COVID-19 have been confirmed to have renal, cardiovascular, gastrointestinal,
and nervous system problems in addition to pulmonary involvement. The pathogenesis of
SARS-CoV-2 is being investigated, but it is possible that the organ damage might in part be caused by
direct viral damage (detection of inclusion bodies in tissues, such as the kidneys), dysregulation of the
immune system, renin-angiotensin system, bradykinin pathway, and coagulation, as well as host genetic
factors and their polymorphisms, which may affect the disease severity. In this review, an update on
the possible pathogenesis pathways of COVID-19 has been provided. It is hoped that the best care
strategy will be developed for patients with COVID-19 by identifying its pathogenesis pathways.