Abstract
HIV infection exerts profound and perhaps irreversible damage to the gut mucosal-associated lymphoid tissues, resulting in long-lasting changes in the signals required for the coordination of commensal colonization and in perturbations at the compositional and functional level of the gut microbiota. These abnormalities in gut microbial communities appear to affect clinical outcomes, including T-cell recovery, vaccine responses, HIV transmission, cardiovascular disease, and cancer pathogenesis. For example, the microbial signature associated with HIV infection has been shown to induce tryptophan catabolism, affect the butyrate synthesis pathway, impair anti-tumoral immunity and affect oxidative stress, which have also been linked to the pathogenesis of cancer. Furthermore, some of the taxa that are depleted in subjects with HIV have proved to modulate the anti-tumor efficacy of various chemotherapies and immunotherapeutic agents. The aim of this work is to provide a broad overview of recent advances in our knowledge of how HIV might affect the microbiota, with a focus on the pathways shared with cancer pathogenesis.
Highlights
A hallmark of treated HIV infection is sustained, low-level viral inflammation
In a subsequent study combining metagenomic and metatranscriptomic data, we showed that HIV-infected individuals exhibited increased anaerobic catabolism of tryptophan via tryptophanase anaerobic fermentation compared with healthy controls [23]
Beyond the neoplasias directly linked to infectious agents, increasing evidence reveals that microbial communities as a whole play a key role in carcinogenesis by altering the balance of host cell proliferation and apoptosis; hindering anti-tumoral immunity; and influencing the metabolism of host-produced factors, ingested food components, and drugs [68, 69]
Summary
A hallmark of treated HIV infection is sustained, low-level viral inflammation. While the cause of this persistent activation of innate and adaptive immunity despite well-controlled HIV RNA replication is not completely understood, it is widely assumed that chronic defects of mucosal immunity are a major contributor [1]. HIV targets the mucosa on structural and functional levels [2,3,4] These disturbances will have consequences on the signals required for the coordination of commensal colonization, which may explain the shifts in microbial distributions and metabolic activity of gut microbial communities [5,6,7]. It is widely accepted that sustained low-level activation of the innate and adaptive immune systems is a major driver of AIDS and non-AIDS-related comorbidities [11,12,13,14,15] These observations argue that microbial translocation, a phenomenon intrinsically linked to the gut microbiota, is a driver of inflammation, and adverse outcomes during treated HIV infection
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