ArticleVirology journal2024
Causal relationships between gut microbiota, plasma metabolites, and HIV infection: insights from Mendelian randomization and mediation analysis.
Article in Virology journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Causal relationships between hundreds of plasma metabolites and PTSD: a bidirectional mendelian randomization study.BMC psychiatry · 2025Pooled it
- Longitudinal trends and causal relationships of depression, anxiety, and sleep quality among MSM newly diagnosed with HIV.Social psychiatry and psychiatric epidemiology · 2026Article
- Association Between Gut Microbiota and HIV Infection Risk: Insights from Mendelian Randomization and 16S rRNA Amplicon Sequencing.Microorganisms · 2026Article
- A taxon-specific measurement of disruption in a multi-modal study of microbiomes and metabolomes reveals system-wide dysbiosis preceding HIV-1 infection.Nature communications · 2025Article
- High-risk Sexual Behavior for HIV Acquisition is Associated with Gut Microbial Community in Men Who Have Sex with Men.Open forum infectious diseases · 2025Article
- Global trends, age-period-cohort analysis, and future projections of diarrhea burden: Findings from the Global Burden of Disease Study 2021.Biosafety and health · 2025Article
- Review
- Bone Loss and Fractures in Post-Menopausal Women Living with HIV: A Narrative Review.Pathogens (Basel, Switzerland) · 2024Review
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3 authors.
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Abstract
objectiveGut dysbiosis and metabolic abnormalities have been implicated in HIV infection. However, the exact causal relationships among the gut microbiota, metabolites, and HIV infection remain poorly understood. Our study involving Mendelian randomization (MR) and mediation analysis aims to unveil these causalities.
methodsGenetic instrumental variables for the gut microbiota were retrieved from MiBioGen consortium (n = 18,340). Metabolism-related genetic variants were sourced from the CLSA cohort (n = 8299). GWAS summary statistics for symptomatic HIV infection were derived from the FinnGen study (n = 309,154), and the UK Biobank (n = 208,808). We performed the bidirectional two-sample MR to assess causalities with the inverse-variance weighted (IVW) method as the primary analysis. Moreover, we executed a mediation analysis using two-step MR methods.
resultsCompared to the causal effects of HIV infection on gut microbiota (or metabolites), those of gut microbiota (or plasma metabolites) on the risk of HIV infection were more substantial. Phylum Proteobacteria (OR: 2.114, 95% CI 1.042-4.288, P = 0.038), and genus Ruminococcaceae UCG013 (OR: 2.127, 95% CI 1.080-4.191, P = 0.029) exhibited an adverse causal effect on HIV infection, whereas genus Clostridium sensu stricto 1(OR: 0.491, 95% CI 0.252-0.956, P = 0.036) and family Erysipelotrichaceae (OR: 0.399, 95% CI 0.193-0.827, P = 0.013) acted as significant protective factors for HIV. The salicyluric glucuronide level (OR = 2.233, 95% CI 1.120-4.453, P = 0.023) exhibited a considerably adverse causal effect on HIV infection. Conversely, the salicylate-to-citrate ratio (OR: 0.417, 95% CI 0.253-0.688, P = 0.001) was identified as a protective factor for HIV. We identified only one bidirectional causality between 1-palmitoyl-GPI and HIV infection. Mechanistically, genus Haemophilus mediated the causal effects of three phospholipids on HIV infection risk: 1-palmitoyl-GPI (mediation proportion = 33.7%, P = 0.018), 1-palmitoyl-2-arachidonoyl-GPI (mediation proportion = 18.3%, P = 0.019), and 1-linoleoyl-2-linolenoyl-GPC (mediation proportion = 20.3%, P = 0.0216). Additionally, 5-Dodecenoylcarnitine (C12:1) mediated the causal effect of genus Sellimonas on the risk of HIV infection (mediation proportion = 13.7%, P = 0.0348).
conclusionOur study revealed that gut microbiota and metabolites causally influence HIV infection risk more substantially than the reverse. We identified the bidirectional causality between 1-palmitoyl-GPI (16:0) and HIV infection, and elucidated four mediation relationships. These findings provide genetic insights into prediction, prevention, and personalized medicine of HIV infection.
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