Microbial translocation contributes to persistent inflammation in both treated and untreated HIV infection. Although translocation is due in part to a disintegration of the intestinal epithelial barrier, there is a bias towards the translocation of Proteobacteria. We hypothesized that intestinal epithelial microvesicle cargo differs after HIV infection and contributes to biased translocation. We isolated gastrointestinal luminal microvesicles before and after progressive simian immunodeficiency virus (SIV) infection in rhesus macaques and measured miRNA and antimicrobial peptide content. We demonstrate that these microvesicles display decreased miR-28-5p, -484, -584-3p, and -584-5p, and let-7b-3p, as well as increased beta-defensin 1 after SIV infection. We further observed dose-dependent growth sensitivity of commensal Lactobacillus salivarius upon co-culture with isolated microvesicles. Infection-associated microvesicle differences were not mirrored in non-progressively SIV-infected sooty mangabeys. Our findings describe novel alterations of antimicrobial control after progressive SIV infection that influence the growth of translocating bacterial taxa. These studies may lead to the development of novel therapeutics for treating chronic HIV infection, microbial translocation, and inflammation.

微生物易位有助于治疗和未治疗的 HIV 感染的持续炎症。尽管易位部分是由于肠上皮屏障的崩解，但变形杆菌的易位存在偏差。我们假设肠上皮微泡货物在 HIV 感染后有所不同，并有助于偏向易位。我们在恒河猴进行性猿猴免疫缺陷病毒 (SIV) 感染前后分离了胃肠道腔微泡，并测量了 miRNA 和抗菌肽的含量。我们证明这些微泡在 SIV 感染后显示 miR-28-5p、-484、-584-3p、-584-5p 和 let-7b-3p 减少，以及 β-防御素 1 增加。我们进一步观察了共生菌的剂量依赖性生长敏感性唾液乳杆菌与分离的微泡共培养。感染相关的微泡差异并未反映在非进行性 SIV 感染的黑眉猴中。我们的研究结果描述了进行性 SIV 感染后抗菌控制的新变化，这些变化影响易位细菌类群的生长。这些研究可能会导致开发治疗慢性 HIV 感染、微生物移位和炎症的新疗法。