The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a positive-sense, single-stranded RNA virus that causes the potentially lethal Covid-19 respiratory tract infection. It does so by binding to host cell angiotensin converting enzyme 2 (ACE2) receptors, leading to endocytosis with the receptor, and subsequently using the host cell’s machinery to replicate copies of itself and invade new cells. The extent of the spread of infection in the body is dependent on the pattern of ACE2 expression and overreaction of the immune system. Additionally, by inducing an imbalance in the renin-angiotensin-aldosterone system (RAAS) and the loss of ACE2 would favour the progression of inflammatory and thrombotic processes in the lungs. No drug or vaccine has yet been approved to treat human coronaviruses. Hundreds of clinical trials on existing approved drugs from different classes acting on a multitude of targets in the virus life cycle are ongoing to examine potential effectiveness for the prevention and treatment of the infection. This review summarizes the SARS-CoV-2 virus life cycle in the host cell and provides a biological and pathological point of view for repurposed and experimental drugs for this novel coronavirus. The viral life cycle provides potential targets for drug therapy. Graphical abstract Unlabelled Image Highlights • ACE2 is a cellular functional receptor for SARS-CoV-2. • Ang (1-7) counterbalances the adverse actions of Ang II on the heart and blood vessels. • The ss-positive sense RNA undergoes translation by using host cell machinery. • Cell attachment, translation, replication and inflammation are drug targets for Covid-19. • The RAAS inhibitors in the pathogenesis of Covid-19 is overly complex and controversial.
【저자키워드】 COVID-19, SARS-CoV-2, ACE2, Remdesivir, immunomodulators, Ang (1-7),