Alterations of the gut microbiota in coronavirus disease 2019 and its therapeutic potential

Figure 1 Potential pathways and mechanisms of gut infection and dysbiosis induced by severe acute respiratory syndrome coronavirus 2. Fecal-oral transmission of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in contaminated water and food, or by swallowing virus-laced sputum, results in gut infection and dysbiosis. SARS-CoV-2 infects alveolar type 2 cells and damages lung tissue before invading the gut through circulating immune cells and the lymphatic system and infiltrating gut epithelial cells via angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2, subsequently triggering gut inflammation and further promoting dysbiosis. Internalization of SARS-CoV-2 Leads to downregulation of ACE2, resulting in inhibition of mechanistic target of rapamycin and subsequent activation of gut autophagy, which modulates the gut microbiome. However, gut microbiota top associations with disease severity in coronavirus disease 2019 patients, such as Coprobacillus, have been shown to upregulate ACE2 expression in the gut. The improper use of antibiotics can also lead to dysbiosis. TMPRSS2: Transmembrane serine protease 2; ACE2: Angiotensin-converting enzyme 2; SARS-CoV-2: Severe acute respiratory syndrome coronavirus 2; mTOR: Mechanistic target of rapamycin.