Immune status, and not HIV infection or exposure, drives the development of the oral microbiota.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
02 07 2020
Historique:
received: 23 03 2020
accepted: 06 06 2020
entrez: 4 7 2020
pubmed: 4 7 2020
medline: 10 2 2021
Statut: epublish

Résumé

Even with antiretroviral therapy, children born to HIV-infected (HI) mothers are at a higher risk of early-life infections and morbidities including dental disease. The increased risk of dental caries in HI children suggest immune-mediated changes in oral bacterial communities, however, the impact of perinatal HIV exposure on the oral microbiota remains unclear. We hypothesized that the oral microbiota of HI and perinatally HIV-exposed-but-uninfected (HEU) children will significantly differ from HIV-unexposed-and-uninfected (HUU) children. Saliva samples from 286 child-participants in Nigeria, aged ≤ 6 years, were analyzed using 16S rRNA gene sequencing. Perinatal HIV infection was significantly associated with community composition (HI vs. HUU-p = 0.04; HEU vs. HUU-p = 0.11) however, immune status had stronger impacts on bacterial profiles (p < 0.001). We observed age-stratified associations of perinatal HIV exposure on community composition, with HEU children differing from HUU children in early life but HEU children becoming more similar to HUU children with age. Our findings suggest that, regardless of age, HIV infection or exposure, low CD4 levels persistently alter the oral microbiota during this critical developmental period. Data also indicates that, while HIV infection clearly shapes the developing infant oral microbiome, the effect of perinatal exposure (without infection) appears transient.

Identifiants

pubmed: 32616727
doi: 10.1038/s41598-020-67487-4
pii: 10.1038/s41598-020-67487-4
pmc: PMC7331591
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

10830

Subventions

Organisme : FIC NIH HHS
ID : D43 TW001041
Pays : United States
Organisme : NIDCR NIH HHS
ID : R01 DE025174
Pays : United States
Organisme : NIH HHS
ID : R01DE025174
Pays : United States
Organisme : FIC NIH HHS
ID : D43TW01041
Pays : United States

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Auteurs

M O Coker (MO)

Department of Oral Biology, Rutgers School of Dental Medicine, 110 Bergen Street, Room C-845, Newark, NJ, 07103, USA. mc2190@sdm.rutgers.edu.
Institute of Human Virology, University of Maryland School of Medicine, Baltimore, MD, USA. mc2190@sdm.rutgers.edu.
Institute of Human Virology Nigeria, Abuja, Nigeria. mc2190@sdm.rutgers.edu.

E F Mongodin (EF)

Institute for Genome Sciences, University of Maryland School of Medicine, Baltimore, USA.

S S El-Kamary (SS)

Department of Epidemiology and Public Health, University of Maryland School of Medicine, Baltimore, MD, USA.

P Akhigbe (P)

Institute of Human Virology Nigeria, Abuja, Nigeria.

O Obuekwe (O)

University of Benin Teaching Hospital, Benin, Nigeria.

A Omoigberale (A)

University of Benin Teaching Hospital, Benin, Nigeria.

P Langenberg (P)

Department of Epidemiology and Public Health, University of Maryland School of Medicine, Baltimore, MD, USA.

C Enwonwu (C)

Department of Microbial Pathogenesis, University of Maryland Dental School, Baltimore, MD, USA.

L Hittle (L)

Institute for Genome Sciences, University of Maryland School of Medicine, Baltimore, USA.

W A Blattner (WA)

Institute of Human Virology, University of Maryland School of Medicine, Baltimore, MD, USA.
Department of Epidemiology and Public Health, University of Maryland School of Medicine, Baltimore, MD, USA.

M Charurat (M)

Institute of Human Virology, University of Maryland School of Medicine, Baltimore, MD, USA.
Department of Epidemiology and Public Health, University of Maryland School of Medicine, Baltimore, MD, USA.

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