Molecular Aspects of Co-morbidities in COVID-19 Infection

Abstract

Coronaviruses are a group of enveloped viruses with single-stranded non-segmented positive-sense RNA genomes. In December 2019, SARS-CoV-2 appeared in China for the first time and quickly spread throughout the world. Although certain medications suggested for other afflictions tend to be potentially effective for curing the infection, there is no approved vaccination or drug available for this virus yet. Comprehension of the disease molecular pathogenesis could provide useful tools for COVID-19 patients in surveillance, prognosis, treatment, vaccine development and therapeutic targeting. The present research aims to summarize the association in COVID-19 patients between molecular dimensions of comorbidities with clinical and preclinical information. Developing an ACE2 inhibitor could be a possible therapeutic target. Plasmin is another possible candidate both in diagnosis and treatment areas. All predicted biomarkers must be validated either through randomized clinical trials or experimental assays before clinical application in patients.

Keywords: COVID-19; Cancer; ardiovascular; hronic obstructive pulmonary disease; iabetes mellitus; ypertension.

Figure 1

Role of plasmin(ogen) in molecular pathogenesis of COVID-19. Plasmin break down Furin-like cleavage site on 682RRAR/S686 of COVID-19 S-glycoprotein underlying increase the ability of attachment between COVID-19 and its human host cell receptor, ACE2, result in virus attachment and fusion. Plasmin also can cleave fibrin and produce D-dimer both in bronchoalveolar lavage fluid and plasma, result in hemorrhage. γENaC is located on apical surface of alveolar epithelium and is responsible for Na+ entrance to epithelial cells. Plasmin cleaves γENaC both on respiratory epithelium and endothelium of veins results in dehydration of respiratory epithelium and hypertension