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Clin Infect Dis. 2020 Jan 2. pii: ciz1235. doi: 10.1093/cid/ciz1235. [Epub ahead of print]

Impact of Hiv-Related Gut Microbiota Alterations on Metabolic Comorbidities.

Author information

1
Viro-immunology Research Unit, Department of Infectious Diseases 8632, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
2
Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
3
Research Institute of Internal Medicine, Division of Surgery, Inflammatory Diseases and Transplantation, Oslo University Hospital Rikshospitalet, Oslo, Norway.
4
Norwegian PSC Research Center, Department of Transplantation Medicine, Oslo University Hospital Rikshospitalet, Oslo Norway.
5
Department of Microbiology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
6
Center for inflammation and Metabolism, Rigshospitalet.
7
Department of pulmonary and infectious diseases, Nordsjællands Hospital, Hillerød, Denmark.
8
Department of Infectious Diseases, Hvidovre Hospital, Copenhagen University Hospital, Copenhagen, Denmark.
9
Medical Department, Lovisenberg Hospital, Oslo.
10
CHIP, Department of Infectious Diseases 8632, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
11
Section of Gastroenterology, Department of Transplantation Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.
12
Section of clinical immunology and infectious diseases, Department of Rheumatology, Dermatology and Infectious diseases, Oslo, Norway.

Abstract

BACKGROUND:

We aimed to identify an HIV-related microbiota signature, independent of sexual preferences and demographic confounders, in order to assess a possible impact of the microbiome on metabolic comorbidites.

METHODS:

Bacterial 16S rRNA analyses were performed on stool samples from 405 HIV-infected and 111 uninfected participants of the Copenhagen Comorbidity in HIV infection (COCOMO) study. Individuals were stratified according to sexual behaviour (men who have sex with men, MSM and non-MSM).

RESULTS:

After excluding MSM-associated microbiota traits and adjusting for confounders, we identified an HIV-related microbiota signature, consisting of lower biodiversity, increased relative abundance of the bacterial clades Gammaproteobacteria and Desulfovibrionaceae and decrease in several Clostridia. This microbiota profile was associated with a 2-fold excess risk of metabolic syndrome, driven by increase in Desulfovibrionaceae and decrease in Clostridia (Butyrivibrio, Coprococcus-2, Lachnospiraceae UCG-001 and CAG-56). This association was accentuated (5-fold excess risk) in individuals with previous severe immunodeficiency, which also modified the association between HIV-related microbiota signature and visceral adipose tissue (VAT) area (p-interaction 0.012). Accordingly, HIV-related microbiota was associated with 30 cm2 larger VAT in individuals with history of severe immunodeficiency, but not in those without.

CONCLUSION:

The HIV-related microbiota was associated with increased risk of metabolic syndrome and VAT accumulation, particularly in individuals with previous severe immunodeficiency, driven by increased Desulfovibrionaceae and lower abundance of several Clostridia. Our findings suggest a potential interplay between HIV-related microbiota, immune dysfunction and metabolic comorbidities. Interventions targeting the gut microbiome may be warranted to reduce cardiovascular risk, particularly in individuals with previous immunodeficiency.

PMID:
31894240
DOI:
10.1093/cid/ciz1235

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