Home Research Feeds A gut microbiome signature for HIV and metabolic dysfunction-associated steatotic liver disease

A gut microbiome signature for HIV and metabolic dysfunction-associated steatotic liver diseaseOriginal paper

Researched by:

  • Karen Pendergrass

Last Updated: 2026-07-05

Karen Pendergrass
Karen Pendergrass

Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease, four years before the first published case study.

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Location
Spain
Sample Site
Feces
Species
Homo sapiens

What was studied?

This study characterized the gut microbiome in people with HIV who also have metabolic dysfunction-associated steatotic liver disease (MASLD). It used 16S rRNA sequencing of the V3-V4 region on stool. Investigators compared three groups to separate the effect of MASLD from HIV. They measured alpha diversity, beta diversity, and genus-level markers. The aim was to find a microbiome signature specific to MASLD in this population.

Who was studied?

The cohort was 80 adults recruited in Madrid, Spain. It included 30 with HIV plus MASLD, 30 with HIV without MASLD, and 20 with MASLD without HIV. All HIV-positive participants were on stable antiretroviral therapy, averaging about six years, with more men than the MASLD-only group. MASLD severity was matched by FibroScan. The design was a multicenter prospective cohort with strict exclusions for active viral hepatitis and heavy alcohol use.

What were the most important findings?

Major butyrate producers, including Faecalibacterium, Ruminococcus, and Lachnospira, dominated all three groups. Shannon and Simpson diversity were higher in MASLD-positive participants (Kruskal-Wallis p = 0.047). Beta diversity separated by MASLD, with MASLD-positive people overlapping regardless of HIV status (ADONIS R squared = 0.166, p < 0.001). MASLD, not HIV, drove community structure (q = 0.002 versus q = 0.930). The Firmicutes/Bacteroidetes ratio did not differ (p = 0.203).

What are the greatest implications of this study?

The findings indicate MASLD influences the gut microbiome more than HIV status alone. Some shifts previously blamed on HIV may instead reflect the high prevalence of fatty liver in this group. The study is cross-sectional and small, so it cannot prove the microbiome causes MASLD. It lacked a fully healthy control group and assessed composition, not microbial function.

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