Gut Microbiome in HIV Pathogenesis: Dysbiosis, Immune Dysfunction, and Viral Persistence
Narrative review synthesizes evidence that gut dysbiosis in HIV infection perpetuates systemic inflammation, impairs immune reconstitution, and may sustain latent viral reservoirs despite effective ART.
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What the study showed
Early HIV replication in the GALT triggers a self-reinforcing cycle of CD4+ T-cell depletion, epithelial barrier breakdown, and microbial translocation that persists under ART. Dysbiosis is characterized by loss of butyrate-producing commensals and enrichment of pro-inflammatory taxa, alongside disruptions in SCFAs and tryptophan catabolites. These changes are associated with residual immune activation and incomplete viral reservoir clearance.
How it was done
Narrative review consolidating current literature on microbiome-HIV interactions, incorporating multi-omics technologies and experimental models including gnotobiotic and humanized mice and intestinal organoids.
Risk of bias
As a narrative review without formal meta-analysis, no quantitative synthesis or systematic bias assessment is provided. Selection criteria for included studies are not described in the abstract, limiting reproducibility.
What this study does NOT prove
The review does not establish direct causality between any specific dysbiotic pattern and viral persistence, nor efficacy of microbiome interventions on HIV clinical outcomes.
In clinical practice
No direct therapeutic recommendation can be derived; findings underscore the relevance of intestinal health monitoring in HIV patients on ART without pointing to validated microbiome-based interventions.
Limitations
As a narrative review without formal meta-analysis, no quantitative synthesis or systematic bias assessment is provided. Selection criteria for included studies are not described in the abstract, limiting reproducibility.
Technical appendix
Version history
- 1.0 · 2026-07-22 — Auto-generated under Evidence Standard v1.0
Paid access: structured summary from public metadata; consult the original study at the source.