Impact of Acute HIV Infection and Early Antiretroviral Therapy on the Human Gut Microbiome.

ART HIV immune activation inflammation microbiome

Journal

Open forum infectious diseases
ISSN: 2328-8957
Titre abrégé: Open Forum Infect Dis
Pays: United States
ID NLM: 101637045

Informations de publication

Date de publication:
12 2020
Historique:
received: 17 06 2019
accepted: 19 08 2019
entrez: 16 12 2020
pubmed: 21 8 2019
medline: 21 8 2019
Statut: epublish

Résumé

Intestinal microbial dysbiosis is evident in chronic HIV-infected individuals and may underlie inflammation that persists even during antiretroviral therapy (ART). It remains unclear, however, how early after HIV infection gut dysbiosis emerges and how it is affected by early ART. Fecal microbiota were studied by 16s rDNA sequencing in 52 Thai men who have sex with men (MSM), at diagnosis of acute HIV infection (AHI), Fiebig Stages 1-5 (F1-5), and after 6 months of ART initiation, and in 7 Thai MSM HIV-uninfected controls. Dysbiotic bacterial taxa were associated with relevant inflammatory markers. Fecal microbiota profiling of AHI pre-ART vs HIV-uninfected controls showed a mild dysbiosis. Transition from F1-3 of acute infection was characterized by enrichment in pro-inflammatory bacteria. Lower proportions of Bacteroidetes and higher frequencies of Proteobacteria and Fusobacteria members were observed post-ART compared with pre-ART. Fusobacteria members were positively correlated with levels of soluble CD14 in AHI post-ART. Evidence of gut dysbiosis was observed during early acute HIV infection and was partially restored upon early ART initiation. The association of dysbiotic bacterial taxa with inflammatory markers suggests that a potential relationship between altered gut microbiota and systemic inflammation may also be established during AHI.

Sections du résumé

Background
Intestinal microbial dysbiosis is evident in chronic HIV-infected individuals and may underlie inflammation that persists even during antiretroviral therapy (ART). It remains unclear, however, how early after HIV infection gut dysbiosis emerges and how it is affected by early ART.
Methods
Fecal microbiota were studied by 16s rDNA sequencing in 52 Thai men who have sex with men (MSM), at diagnosis of acute HIV infection (AHI), Fiebig Stages 1-5 (F1-5), and after 6 months of ART initiation, and in 7 Thai MSM HIV-uninfected controls. Dysbiotic bacterial taxa were associated with relevant inflammatory markers.
Results
Fecal microbiota profiling of AHI pre-ART vs HIV-uninfected controls showed a mild dysbiosis. Transition from F1-3 of acute infection was characterized by enrichment in pro-inflammatory bacteria. Lower proportions of Bacteroidetes and higher frequencies of Proteobacteria and Fusobacteria members were observed post-ART compared with pre-ART. Fusobacteria members were positively correlated with levels of soluble CD14 in AHI post-ART.
Conclusions
Evidence of gut dysbiosis was observed during early acute HIV infection and was partially restored upon early ART initiation. The association of dysbiotic bacterial taxa with inflammatory markers suggests that a potential relationship between altered gut microbiota and systemic inflammation may also be established during AHI.

Identifiants

pubmed: 33324725
doi: 10.1093/ofid/ofz367
pii: ofz367
pmc: PMC7724511
doi:

Types de publication

Journal Article

Langues

eng

Pagination

ofz367

Subventions

Organisme : CCR NIH HHS
ID : HHSN261200800001C
Pays : United States
Organisme : NCI NIH HHS
ID : HHSN261200800001E
Pays : United States

Investigateurs

Nipat Teeratakulpisarn (N)
Supanit Pattanachaiwit (S)
Mark de Souza (M)
James Fletcher (J)
Eugene Kroon (E)
Ponpen Tantivitayakul (P)
Duanghathai Suttichom (D)
Somprartthana Rattanamanee (S)
Kultida Poltavee (K)
Jintana Intasan (J)
Tassanee Luekasemsuk (T)
Hathairat Savadsuk (H)
Somporn Tipsuk (S)
Suwanna Puttamsawin (S)
Khunthalee Benjapornpong (K)
Nisakorn Ratnaratorn (N)
Patcharin Eamyoung (P)
Sasiwimol Ubolyam (S)
Robert O'Connell (R)
Siriwat Akapirat (S)
Bessara Nuntapinit (B)
Nantana Tantibul (N)
Nampueng Churikanont (N)
Saowanit Getchalarat (S)
Sandhya Vasan (S)
Rapee Trichavaroj (R)
Chayada Sajiaweerawan (C)
Yuwadee Phuang-Ngern (Y)
Surat Jongrakthaitae (S)
Suchada Sukhumvittaya (S)
Putida Saetun (P)
Weerawan Chuenarom (W)
Nelson Michael (N)
Ellen Turk (E)
Corinne McCullough (C)
Oratai Butterworth (O)
Mark Milazzo (M)

Commentaires et corrections

Type : ErratumIn

Informations de copyright

Published by Oxford University Press on behalf of Infectious Diseases Society of America 2019.

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Auteurs

Ornella Sortino (O)

Clinical Research Directorate, Frederick National Laboratory for Cancer Research, sponsored by the National Cancer Institute.
National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland.

Nittaya Phanuphak (N)

SEARCH/Thai Red Cross AIDS Research Centre, Bangkok, Thailand.

Alexandra Schuetz (A)

The Henry M. Jackson Foundation for the Advancement of Military Medicine, Bethesda, Maryland.
United States Military HIV Research Program, Walter Reed Army Institute of Research, Silver Spring, Maryland.
Armed Forces Research Institute of Medical Sciences, Bangkok, Thailand.

Alexandra M Ortiz (AM)

National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland.

Nitiya Chomchey (N)

SEARCH/Thai Red Cross AIDS Research Centre, Bangkok, Thailand.

Yasmine Belkaid (Y)

Metaorganism Immunity Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland.
Microbiome Program, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland.

Jacquice Davis (J)

Microbiome Program, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland.

Harry A Mystakelis (HA)

National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland.

Mariam Quiñones (M)

Bioinformatics and Computational Biosciences Branch, Office of Cyber Infrastructure and Computational Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland.

Claire Deleage (C)

Clinical Research Directorate, Frederick National Laboratory for Cancer Research, sponsored by the National Cancer Institute.

Brian Ingram (B)

Metabolon, Inc., Research Triangle Park, North Carolina.

Rungsun Rerknimitr (R)

SEARCH/Thai Red Cross AIDS Research Centre, Bangkok, Thailand.

Suteeraporn Pinyakorn (S)

The Henry M. Jackson Foundation for the Advancement of Military Medicine, Bethesda, Maryland.
United States Military HIV Research Program, Walter Reed Army Institute of Research, Silver Spring, Maryland.

Adam Rupert (A)

Clinical Research Directorate, Frederick National Laboratory for Cancer Research, sponsored by the National Cancer Institute.

Merlin L Robb (ML)

The Henry M. Jackson Foundation for the Advancement of Military Medicine, Bethesda, Maryland.
United States Military HIV Research Program, Walter Reed Army Institute of Research, Silver Spring, Maryland.

Jintanat Ananworanich (J)

The Henry M. Jackson Foundation for the Advancement of Military Medicine, Bethesda, Maryland.
United States Military HIV Research Program, Walter Reed Army Institute of Research, Silver Spring, Maryland.
Department of Global Health, University of Amsterdam, Amsterdam, the Netherlands.

Jason Brenchley (J)

National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland.

Irini Sereti (I)

National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland.

Classifications MeSH