ArticleScience translational medicine2013
Dysbiosis of the gut microbiota is associated with HIV disease progression and tryptophan catabolism.
Article in Science translational medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. It is linked to trial NCT02256592 (Reconstitution of the Gut Microbiome to Reduce HIV-Associated Inflammation), which is not on this map. Cited by 466 papers, 3 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Reconstitution of the Gut Microbiome to Reduce HIV-Associated Inflammation
Who cites it
466 citing papers in PubMed, 3 syntheses or guidelines pooled it, 746 citations in OpenAlex.
- Pooled it
- Effects ofFrontiers in nutrition · 2025Pooled it
- HIV and the gut microbiome: future research hotspots and trends.Frontiers in microbiology · 2025Pooled it
- Dolutegravir restores gut microbiota in late-stage HIV-1 unlike darunavir: an open-label, randomized clinical trial.Nature communications · 2026Trial
- Interactions between gut microbiota, plasma metabolome and brain function in the setting of a HIV cure trial.Frontiers in cellular and infection microbiology · 2025Trial
- Fecal microbiota transplantation alters the proteomic landscape of inflammation in HIV: identifying bacterial drivers.Microbiome · 2024Trial
- Targeting the Gut Microbiota of Vertically HIV-Infected Children to Decrease Inflammation and Immunoactivation: A Pilot Clinical Trial.Nutrients · 2022Trial
- Probiotic effects on immunity and microbiome in HIV-1 discordant patients.Frontiers in immunology · 2022Trial
- Fecal microbiota transplantation in HIV: A pilot placebo-controlled study.Nature communications · 2021Trial
- Microbial metabolite-driven mechanisms linking the gut microbiome to atherosclerosis: multi-omic and translational perspectives.Gut microbes · 2026Review
- Latent tuberculosis infection shapes gut microbiome and immune-metabolic interactions in people living with HIV.Gut microbes · 2026Article
- Higher plasma kynurenine-tryptophan ratio predicts incident hepatic fibrosis in women with HIV.AIDS (London, England) · 2026Article
- Expansion of pathogens and restoration of human skin microbiome in CD4 T-cell lymphopenia.The Journal of investigative dermatology · 2026Article
- Mucosal-associated invariant T cells respond to colonic microbiome alterations during acute HIV infection.Mucosal immunology · 2026Article
- Tryptophan metabolism in colorectal cancer: From mechanistic insights to novel therapeutic strategies.Clinical and translational medicine · 2026Review
- Interaction of the Gut Microbiota and the Enteric Nervous System: Implications in Gastrointestinal Disorders Associated With Autism Spectrum Disorder.Autism research : official journal of the International Society for Autism Research · 2026Review
- HIV cure after HCT: 7 horses seem to be on the mark.Blood advances · 2026Article
- Senescence-associated loss of intestinal α1,2-fucose disrupts a modifiable host-microbiome homeostasis axis in people with HIV.bioRxiv : the preprint server for biology · 2026Article
- Integrating host-microbiota metabolic networks: how aromatic amino acids shape immune homeostasis and affect disease progression.Cellular & molecular immunology · 2026Review
- HIV Infection and Opioid Treatment Enable the Engraftment of Kaposi Sarcoma-Like Tumors Into Immunocompetent Mice.Journal of medical virology · 2026Article
406 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
Progressive HIV infection is characterized by dysregulation of the intestinal immune barrier, translocation of immunostimulatory microbial products, and chronic systemic inflammation that is thought to drive progression of disease to AIDS. Elements of this pathologic process persist despite viral suppression during highly active antiretroviral therapy (HAART), and drivers of these phenomena remain poorly understood. Disrupted intestinal immunity can precipitate dysbiosis that induces chronic inflammation in the mucosa and periphery of mice. However, putative microbial drivers of HIV-associated immunopathology versus recovery have not been identified in humans. Using high-resolution bacterial community profiling, we identified a dysbiotic mucosal-adherent community enriched in Proteobacteria and depleted of Bacteroidia members that was associated with markers of mucosal immune disruption, T cell activation, and chronic inflammation in HIV-infected subjects. Furthermore, this dysbiosis was evident among HIV-infected subjects undergoing HAART, and the extent of dysbiosis correlated with activity of the kynurenine pathway of tryptophan catabolism and plasma concentrations of the inflammatory cytokine interleukin-6 (IL-6), two established markers of disease progression. Gut-resident bacteria with capacity to catabolize tryptophan through the kynurenine pathway were found to be enriched in HIV-infected subjects, strongly correlated with kynurenine levels in HIV-infected subjects, and capable of kynurenine production in vitro. These observations demonstrate a link between mucosal-adherent colonic bacteria and immunopathogenesis during progressive HIV infection that is apparent even in the setting of viral suppression during HAART. This link suggests that gut-resident microbial populations may influence intestinal homeostasis during HIV disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.