Figure 1.

The figure shows how the pathogenesis of SARS-CoV-2 affects the microbiome. The diagram shows that in people already predisposed toward the disease due to age, comorbidities, and environmental factors like pollution, diet, and microbiome, the pathogenesis is facilitated due to prior downregulation of the ACE2 receptor, which is the major receptor for SARS-CoV-2 entry into the lung epithelia. On viral entry, ACE2 is further downregulated and initiates a cascade of events like dysregulation of RAS, slows conversion of AngII to Ang 1-7, upregulation of the ACE-Ang-II-AT₁R axis (indicated by *** in the figure) and downregulation of the ACE-2-Ang-(1-7)-Mas axis (indicated by * in the figure), leading to clinical symptoms like an increase in blood pressure, imbalance of fluids and electrolytes, oxidative stress, vascular permeability alterations, and eventually increase in inflammation leading to the cytokine storm accentuated by the activation of NF-κβ, MAPK pathway, and finally leading to lung damage. Downregulation of ACE2 also leads to the absence of the tryptophan transporter B°AT1 leading to the inhibition of tryptophan uptake, which consequently leads to the reduction of the mTOR pathway, impaired expression of antimicrobial peptides (AMPs), and increase in autophagy leading to diarrhea and dysbiosis of the microbiome. Microbiome dysbiosis in COVID-19 has been found to be characterized by the upsurge of certain taxa and decrease of others, as indicated in Table 2 .