Figure 1.

Proposed mechanisms of gut dysbiosis and microbial translocation in the GI tract with HIV (1). HIV causes dysregulation of immune cells such as dendritic cells, macrophages, and Th17 cells, which increases the growth of dysbiotic communities. Additionally, HIV causes a significant decrease in Th17 cells, a subtype of CD4+ T cells, which normally limit microbial translocation. Loss of Th17 cells leads to a decrease in tight junctions in the intestinal epithelium allowing microbes to travel freely between the lumen and systemic circulation. Loss of Th17 cells also causes an increase in Treg cells, which are associated with suppression of viral clearance and inappropriate tolerance of microbes. (2) Increased translocation of microbes into systemic circulation interferes with expression of the pattern recognition receptor (PRR) which ultimately increases gut inflammation, decreases immune response to viral infection, and increases growth of dysbiotic communities. (3) Increased gut inflammation from HIV infection leads to increased production of oxygen and nitrogen radicals. This is associated with increased growth of facultative anaerobes such as Enterobacteriaceae family.