Several common symptoms of early infection can be the indirect result of epithelial cell necrosis by viral infection mediated by ACE2 and/or other co-receptors, such as transmembrane protease serine 2, (TMPRSS2) [13]. Uptake of virus or epithelial cell debris by lung macrophages can initiate inflammasome activation by P2RX7 and release IL-1β, Type1 IFN, IL-6 and TNF [3], contributing to fever, pain, lethargy and headache. Raised levels of C-reactive protein (CRP), induced in hepatocytes by IL-6, are acute phase, plasma biomarkers of COVID-19. Other macrophage products include chemokines such as IL-8 (CXCL8) and MCP-1 (CCL2), recruiting abundant PMN and monocytes to sites of infection. Through viraemia COVID-19 reaches systemic organs such as heart, gut, brain and kidney, which contain resident and recruited macrophage populations; these contribute to local, specialised dysfunctions, such as myocarditis and cardiac arrhythmia, following interactions of macrophages and infected cardiomyocytes [54]. Intravascular coagulation [3,24] promotes dissemination of microthrombi-emboli to lungs, heart and brain, and fibrin degradation d-dimers appear in blood. This is evidence of early resolution, enhanced by the generation of antiviral IgM and IgG.