Fig. 3.

Mechanisms of virus entry, cell death, immune response, cytokine storm and coronavirus pathogenesis. Following the entrance of the virus through the ACE2 receptor, AngII activates purinergic or pannexin receptors. ROS production following viral infection, through the path shown, eventually induces cell death pathways and organ failure. Activation of Ca++-dependent signaling cascades also facilitates virus entry into the cell through actin polymerization. On the other hand, activation of purinergic and pannexin receptors activates and recruits immune cells. Following this event, inflammatory processes and cytokine storms, with the production of hyaluronan and RBC damage, caused lung damage and lack of oxygen transfer, respectively, which together exacerbate the respiratory symptoms of the COVID-19. ACE2, Angiotensin-converting enzyme 2; AngII, angiotensin II; ATP, Adenosine triphosphate; COVID-19, Coronavirus disease 2019; Panx1, Pannexin 1; PARP1, Poly [ADP-ribose] polymerase 1; RBC, Red blood cells; ROS, Reactive oxygen species; TRMP2, Transient receptor potential cation channel subfamily M member 2. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)