Does mass management of chronic hepatitis C protect the Egyptian population against fulminant coronavirus disease-2019? “Postulating a hypothesis”

Abstract

Coronavirus disease (COVID-19) is caused by the pathogenic virus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Egypt has launched a national treatment program to provide a cure for Egyptian patients infected with hepatitis C virus (HCV). A common mechanism is shared between both the anticipated and unexpected aspects of COVID-19. The activity of the renin-angiotensin system (RAS) is intrinsically high in the lungs, which is a major source of ACE and hence a significant site of systemic synthesis of Ang II. Angiotensin-converting enzyme 2 (ACE2) is the cellular receptor for SARS-CoV-2, the etiological agent of the COVID-19 disease. ACE-2 and its angiotensin 1–7 (Ang 1–7) product, which acts on the Mas oncogene receptor, have been shown to play a protective role in fibrogenesis and inflammation of many organs, including the liver and lung. Antiviral treatment with interferon (IFN) in conjunction with ribavirin in patients with chronic hepatitis C reduces serum ACE activity and indirectly affects liver parenchyma fibrogenesis. The antifibrotic activity of sofosbuvir plus daclatasvir (SOF/DAC) is independent of its antiviral action. Elimination of HCV infection by DAA therapy in patients with chronic hepatitis C could improve natural killer (NK) activity by increasing the frequency of CD 16+ CD 56+ NK cells. COVID-19 individuals exhibit enhanced platelet activation and aggregation, as well as platelet-monocyte aggregation, which is linked to coagulative disorders. Lower systemic inflammation and enhanced hepatic synthesis of both pro- and anti-coagulant factors were noticed soon after antiviral therapy. In order to protect against the severity of COVID-19, treatment of chronic hepatitis C has been observed as a possible key as a prophylaxis beside the vaccine and should be tested for evidence or rejection of observation.