The global outbreak of Coronavirus disease 2019 (COVID-19), caused by the Severe Acute Respiratory Syndrome CoronaVirus 2 (SARS-CoV-2/2019-nCoV) has put forth a serious threat to the international public health and has ruined the global economy. Till date, no drugs have been approved for Coronavirus Disease-2019 (COVID-19), although use of some drugs in trial phase has been attempted. The drugs being used for management of COVID-19 disease include chloroquine (CQ), hydroxychloroquine (HCQ), and remdesivir. In this article, we have aimed to review existing literature and mechanism by which CQ and HCQ have an effect on COVID-19, most importantly by interfering with autophagy, lysosomal activity, receptor binding and membrane fusion. We have systematically searched the PubMed database upto April, 2020 and analysed all the articles published on CQ, HCQ and COVID-19. The available data provides insights into the immunomodulatory potency of HCQ, along with the molecular mechanism of action of the drug on the SARS-CoV-2.
COVID-19 is characterized by fever, cough, shortness of breath, myalgia, and headache. The disease also takes a more severe form with life-threatening manifestations of acute respiratory distress syndrome (ARDS), acute cardiac injury, acute kidney injury, disseminated intravascular coagulopathy, and cytokine storm. It has been elucidated that like its predecessor, the SARS CoV, the SARS CoV-2 utilizes the ACE2 receptor to enter cells. This knowledge brought into speculation the effects of a dysregulated Renin-Angiotensin system (RAS) in the pathogenesis of COVID-19. It has been proposed that the effects of a dysregulated RAS would lead to an inflammatory cascade and contribute to the cytokine storm that is central to the disease. This paper looks at the RAS pathway and the hypothesizes the possibility of a positive RAS feedback loop in the pathogenesis of COVID-19. We also propose possible drug targets for the treatment of COVID-19.