Runtuwene Lucky Ronald, Parbie Prince Kofi, Mizutani Taketoshi, Ishizaka Aya, Matsuoka Saori, Abana Christopher Zaab-Yen, Kushitor Dennis, Bonney Evelyn Yayra, Ofori Sampson Badu, Kiyono Hiroshi, Ishikawa Koichi, Ampofo William Kwabena, Matano Tetsuro
AIDS Research Center, National Institute of Infectious Diseases, Tokyo, Japan.
Graduate School of Frontier Sciences, The University of Tokyo, Kashiwa, Japan.
Front Microbiol. 2024 Feb 15;15:1359402. doi: 10.3389/fmicb.2024.1359402. eCollection 2024.
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 ( and ) and a genus associated with gut protection (). 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.
已知人类免疫缺陷病毒1型(HIV-1)感染会导致肠道微生物群失调。原因之一是HIV-1直接感染肠道驻留的CD4 T细胞,引发一系列现象,导致肠道黏膜不稳定。尽管进行了抗逆转录病毒治疗,但HIV感染对肠道微生物群失调的影响仍未得到解决。在此,我们展示了一项对HIV感染者(PLWH)微生物组分析的纵向研究结果。我们将HIV患者在第一个和第二个时间点(分别为基线病例和六个月后的随访病例)的微生物组多样性和组成与健康个体(基线对照)进行了对比。我们发现,尽管随访病例中的多样性指数较低,但一些属的丰度有所恢复,但未完全恢复到与基线对照相似的水平。一些属在PLWH中始终具有较高的丰度。此外,我们发现CD4 T细胞计数和可溶性CD14水平分别与高和低多样性指数显著相关。我们还发现,一些属的丰度与临床特征高度相关,尤其是与抗逆转录病毒治疗持续时间相关。这包括已知与HIV-1进展较差相关的属(和)以及与肠道保护相关的一个属()。肠道保护因子和与HIV-1进展较差相关的属均富集这一事实可能表明,尽管临床特征有所改善,但肠道黏膜仍受到损害。