Fig. 1: Model of intestinal SARS-CoV-2 infections.

A Possible routes and sites of infection; 1 = infection of nasal epithelium; 2 = alternative oral ingestion of SARS-CoV-2 particles; 3 = gastric passage of infectious SARS-CoV-2 dependent on gastric pH (influenced by proton pump inhibitor intake); 4 = infection of enteric cells and active replication of virus; 5 = fecal shedding of virus or virus parts. B Intestinal tropism of SARS-CoV2 and subsequent changes of mucosal immune composition (I-II) = binding of SARS-CoV2 to luminal angiotensin-converting enzyme 2 (ACE2); transmembrane protease serine subtype (TMPRSS) 2- and TMPRSS4-dependent internalization of SARS-CoV-2 virus; (III) viral replication and virus dependent lysis of epithelial cells, (IV) decrease in inflammatory dendritic cells (V) infiltration with effector CD4⁺ and CD8⁺ T cells; (VI) increased abundance of IEL; (VII) decrease in IL-17 producing cells, (VIII) activation of B cells as well as formation of memory B cells through long-term persistance of SARS-CoV2 in eneterocytes and production of IgM, IgM and IgA.