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Rectal microbiota among HIV-uninfected, untreated HIV, and treated HIV-infected in Nigeria

Nowak, Rebecca G.; Bentzen, Søren M.; Ravel, Jacques; Crowell, Trevor A.; Dauda, Wuese; Ma, Bing; Liu, Hongjie; Blattner, William A.; Baral, Stefan D.; Charurat, Manhattan E.; on behalf of the TRUSTRV368 Study Group

doi: 10.1097/QAD.0000000000001409
Epidemiology and Social: Concise Communication

Objective: Untreated advanced HIV infection alters the gut microbiota, but it is unclear whether antiretroviral therapy (ART) reverses these changes. We compared the composition of the rectal microbiota among three groups of men who have sex with men (MSM): HIV-uninfected, untreated HIV, and ART-treated HIV-infected.

Design: A cross-sectional study was conducted among 130 MSM (55 HIV-uninfected, 41 untreated HIV, and 34 ART-treated HIV) in Abuja, Nigeria.

Methods: Bacterial 16S rRNA genes were amplified from rectal swabs, sequenced and clustered into Genera-level operational taxonomic units. Alpha diversity was quantified using the Shannon index and compared among groups using the Kruskal–Wallis test; associations with other scale variables were quantified using Spearman's rank correlation (Rs). The relative abundance of the top 15 taxa was compared according to HIV infection/treatment status using the Wilcoxon rank sum test.

Results: HIV-treated MSM had a decrease in a commensal phylum, Bacteroidetes (P < 0.01). Alpha diversity was positively correlated with viral loads (Rs = 0.32, P < 0.01). Statistically significant shifts in relative abundance of rectal microbiota for the HIV-treated group included a decrease in the most abundant bacteria, Prevotella (P = 0.02) and an increase in pathogenic bacteria, Peptoniphilus (P = 0.04), Finegoldia (P = 0.01), Anaerococcus (P = 0.03), and Campylobacter (P = 0.03) compared with the other groups.

Conclusion: Untreated HIV infection does not significantly alter the rectal microbiota, whereas prior treatment is associated with a shift toward a more pathogenic pattern of microbiota. Treatment with an antibiotic, co-trimoxazole, in conjunction with ART may have contributed to this shift.

aInstitute of Human Virology, University of Maryland School of Medicine

bUniversity of Maryland Greenebaum Comprehensive Cancer Center

cDepartment of Epidemiology and Public Health

dInstitute for Genome Sciences, University of Maryland School of Medicine, Baltimore

eUS Military HIV Research Program, Walter Reed Army Institute of Research, Silver Spring

fHenry M. Jackson Foundation for the Advancement of Military Medicine, Bethesda, Maryland, USA

gInstitute of Human Virology, Nigeria, Abuja, Nigeria

hSchool of Public Health, University of Maryland, College Park

iJohns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA.

Correspondence to Rebecca G. Nowak, PhD, Institute of Human Virology, University of Maryland School of Medicine, 725 W. Lombard Street, Baltimore, MD 21201, USA. Tel: +1 410 706 4642; fax: +1 410 706 1944; e-mail: rnowak@ihv.umaryland.edu

Received 1 November, 2016

Revised 9 December, 2016

Accepted 10 January, 2017

Copyright © 2017 Wolters Kluwer Health, Inc.