HIV rebound in HIV controllers is associated with a specific fecal microbiome profile.

Fecal microbiome HIV controllers HIV‐1 rebound Immune activation TLR7 Vesatolimod

Journal

European journal of immunology
ISSN: 1521-4141
Titre abrégé: Eur J Immunol
Pays: Germany
ID NLM: 1273201

Informations de publication

Date de publication:
10 May 2024
Historique:
revised: 19 04 2024
received: 27 02 2024
accepted: 30 04 2024
medline: 10 5 2024
pubmed: 10 5 2024
entrez: 10 5 2024
Statut: aheadofprint

Résumé

HIV infection is associated with gut dysbiosis, and microbiome variability may affect HIV control when antiretroviral therapy (ART) is stopped. The TLR7 agonist, vesatolimod, was previously associated with a modest delay in viral rebound following analytical treatment interruption in HIV controllers (HCs). Using a retrospective analysis of fecal samples from HCs treated with vesatolimod or placebo (NCT03060447), people with chronic HIV (CH; NCT02858401) or without HIV (PWOH), we examined fecal microbiome profile in HCs before/after treatment, and in CH and PWOH. Microbiome diversity and abundance were compared between groups to investigate the association between specific phyla/species, immune biomarkers, and viral outcomes during treatment interruption. Although there were no significant differences in gut microbiome diversity between people with and without HIV, HCs, and CH shared common features that distinguished them from PWOH. there was a trend toward greater microbiome diversity among HCs. Treatment with vesatolimod reduced dysbiosis in HCs. Firmicutes positively correlated with T-cell activation, while Bacteroidetes and Euryarchaeota inversely correlated with TLR7-mediated immune activation. Specific types of fecal microbiome abundance (e.g. Alistipes putredinis) positively correlated with HIV rebound. In conclusion, variability in the composition of the fecal microbiome is associated with markers of immune activation following vesatolimod treatment and ART interruption.

Identifiants

pubmed: 38727191
doi: 10.1002/eji.202350809
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

e2350809

Subventions

Organisme : Gilead Sciences

Informations de copyright

© 2024 Wiley‐VCH GmbH.

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Auteurs

Yanhui Cai (Y)

Gilead Sciences, Inc., Foster City, California, USA.

Ondrej Podlaha (O)

Gilead Sciences, Inc., Foster City, California, USA.

Steven G Deeks (SG)

Department of Medicine, University of California San Francisco, San Francisco, California, USA.

Cynthia Brinson (C)

Central Texas Clinical Research, Austin, Texas, USA.

Moti N Ramgopal (MN)

Midway Immunology and Research Center, Fort Pierce, Florida, USA.

Edwin DeJesus (E)

Orlando Immunology Centre, Orlando, Florida, USA.

Anthony Mills (A)

Men's Health Foundation, West Hollywood, California, USA.

Peter Shalit (P)

Peter Shalit MD and Associates, Seattle, Washington, USA.

Mohamed Abdel-Mohsen (M)

Vaccine and Immunotherapy Center, The Wistar Institute, Philadelphia, Pennsylvania, USA.

Liao Zhang (L)

Gilead Sciences, Inc., Foster City, California, USA.

Christiaan R de Vries (CR)

Gilead Sciences, Inc., Foster City, California, USA.

Elena Vendrame (E)

Gilead Sciences, Inc., Foster City, California, USA.

Devi SenGupta (D)

Gilead Sciences, Inc., Foster City, California, USA.

Jeffrey J Wallin (JJ)

Gilead Sciences, Inc., Foster City, California, USA.

Classifications MeSH