Gut microbiome in people living with HIV is associated with impaired thiamine and folate syntheses.
Gut microbiome in people living with HIV is associated with impaired thiamine and folate syntheses.
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DOI：
10.1016/j.micpath.2021.105209
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发表时间：
2021-11
影响因子：
3.8
通讯作者：
Lee HY
中科院分区：
文献类型：
--
作者：
Park SY;Faraci G;Nanda S;Ter-Saakyan S;Love TMT;Mack WJ;Dubé MP;Lee HY
作为通常与炎症有关的共病，艾滋病毒感染者心血管和神经系统疾病的发病率很高。虽然微生物易位可以增加HIV感染期间的炎症，但功能性微生物组的变化可能增加促炎反应尚未得到充分表征。此外，由于个体之间的高度可变性，定义hiv诱导的微生物组变化变得复杂。本文对305例HIV阳性和249例HIV阴性个体的16S核糖体RNA基因序列进行了功能注释，并根据地理区域、性别、性行为和年龄进行了调整。从这些个体的16S数据推断出宏基因组图谱。HIV感染与微生物维生素B合成受损有关；在艾滋病毒阳性组中，大约一半的硫胺素和叶酸生物合成途径基因家族的丰度明显低于阴性对照组。这些结果与艾滋病毒感染中高流行的硫胺素和叶酸缺乏症相一致。鉴于b族维生素缺乏、炎症和这些疾病之间的文献关联，这些hiv诱导的微生物群变化有可能影响心血管和神经认知疾病。我们还观察到hiv感染者微生物组中大多数必需氨基酸生物合成途径下调。当我们比较262例ART阳性和184例ART阴性个体时，抗逆转录病毒治疗没有显著恢复微生物维生素B和氨基酸合成途径。我们的荟萃分析为理解HIV患者的维生素B和氨基酸缺乏提供了新的前景，表明逆转HIV诱导的微生物组变化的干预措施可能有助于减轻HIV合并症的负担。
People living with HIV have a high incidence of cardiovascular and neurological diseases as comorbid disorders that are commonly linked to inflammation. While microbial translocation can augment inflammation during HIV infection, functional microbiome shifts that may increase pro-inflammatory responses have not been fully characterized. In addition, defining HIV-induced microbiome changes has been complicated by high variability among individuals. Here we conducted functional annotation of previously-published 16S ribosomal RNA gene sequences of 305 HIV positive and 249 negative individuals, with adjustment for geographic region, sex, sexual behavior, and age. Metagenome profiles were inferred from these individuals’16S data. HIV infection was associated with impaired microbial vitamin B synthesis; around half of the gene families in thiamine and folate biosynthesis pathways were significantly less abundant in the HIV positive group than the negative control. These results are consistent with the high prevalence of thiamine and folate deficiencies in HIV infections. These HIV-induced microbiota shifts have the potential to influence cardiovascular and neurocognitive diseases, given the documented associations between B-vitamin deficiencies, inflammation, and these diseases. We also observed that most essential amino acid biosynthesis pathways were downregulated in the microbiome of HIV-infected individuals. Microbial vitamin B and amino acid synthesis pathways were not significantly recovered by antiretroviral treatment when we compared 262 ART positive and 184 ART negative individuals. Our meta-analysis provides a new outlook for understanding vitamin B and amino acid deficiencies in HIV patients, suggesting that interventions for reversing HIV-induced microbiome shifts may aid in lessening the burdens of HIV comorbidities.
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