Fig. 2.

Host response to SARS-CoV-2 infection and proposed interplay with intestinal barrier permeability and bacterial translocation. SARS-CoV-2 infection and replication culminate in the activation of innate and adaptive immunity, and complement, with systemic and local effects, e.g. cytokine release syndrome. In addition, IL-6-mediated endothelial cell damage [tissue factor exposure], coagulation, and vasculature leakage induce further tissue damage and perpetuate systemic inflammation. This complex systemic and local pathologic condition may induce intestinal damage and increase the intestinal permeability precipitating intestinal barrier failure and bacterial translocation, which in turn auto-fuel vicious cycles of systemic inflammation and tissue damage. Abbreviations: IL, interleukin; SIL-2R, soluble IL-2 receptor; SIL-6R, soluble IL-6 receptor; GM-CSF, granulocyte-macrophage colony-stimulating factor; IP, interferon gamma-inducible protein; MIP, macrophage inflammatory protein; TLR, tool-like receptor; Th17, T helper 17 cell; DAMPs, damage-associated molecular patterns; PAMPs, pathogen-associated molecular patterns; LPS, lipopolysaccharide.