Longitudinal analysis of microbiome composition in Ghanaians living with HIV-1

Front Microbiol. 2024 Feb 15:15:1359402. doi: 10.3389/fmicb.2024.1359402. eCollection 2024.

Abstract

Human immunodeficiency virus (HIV) 1 infection is known to cause gut microbiota dysbiosis. Among the causes is the direct infection of HIV-1 in gut-resident CD4+ T cells, causing a cascade of phenomena resulting in the instability of the gut mucosa. The effect of HIV infection on gut microbiome dysbiosis remains unresolved despite antiretroviral therapy. Here, we show the results of a longitudinal study of microbiome analysis of people living with HIV (PLWH). We contrasted the diversity and composition of the microbiome of patients with HIV at the first and second time points (baseline_case and six months later follow-up_case, respectively) with those of healthy individuals (baseline_control). We found that despite low diversity indices in the follow-up_case, the abundance of some genera was recovered but not completely, similar to baseline_control. Some genera were consistently in high abundance in PLWH. Furthermore, we found that the CD4+ T-cell count and soluble CD14 level were significantly related to high and low diversity indices, respectively. We also found that the abundance of some genera was highly correlated with clinical features, especially with antiretroviral duration. This includes genera known to be correlated with worse HIV-1 progression (Achromobacter and Stenotrophomonas) and a genus associated with gut protection (Akkermansia). The fact that a protector of the gut and genera linked to a worse progression of HIV-1 are both enriched may signify that despite the improvement of clinical features, the gut mucosa remains compromised.

Keywords: Ghana; HIV; PLWH; gut microbiome dysbiois; longitudinal analysis.

Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This study was supported by Japan Agency for Medical Research and Development (AMED) (grant numbers: JP23fk0410035, JP23wm0125012, JP18fk0410003, JP20fk0410011, JP20fk0108125, JP20fk0108139, JP19kk0205024, JP20jk0210002, JP21am0401029, 223fa627003h0001, and JP21ae0121040), AMED-JICA (the Science and Technology Research Partnership for Sustainable Development [SATREPS]; JP20jm0110012), and the Ministry of Education, Culture, Sports, Science, and Technology in Japan (18H02666). The Kumamoto University International Scholarship Program generously provided travel support during this study.