Even with sustained use of antiretroviral therapy (ART), HIV-infected individuals have an increased risk of systemic comorbid conditions and oral pathologies, including opportunistic infections, oral mucosal inflammation, and gingival and periodontal diseases. The immune-mediated mechanisms that drive this increased risk, in the context of sustained viral suppression, are unclear. HIV infection, even when controlled, alters microbial communities contributing to a chronic low-grade inflammatory state that underlies these non-HIV co-morbidities. The higher prevalence of dental caries, and mucosal and periodontal inflammation reported in HIV-infected individuals on ART is often associated with differentially abundant oral microbial communities, possibly leading to a heightened susceptibility to inflammation. This mini-review highlights current gaps in knowledge regarding the microbe-mediated oral mucosal immunity with HIV infection while discussing opportunities for future research investigations and implementation of novel approaches to elucidate these gaps. Interventions targeting both inflammation and microbial diversity are needed to mitigate oral inflammation-related comorbidities, particularly in HIV-infected individuals. More broadly, additional research is needed to bolster general models of microbiome-mediated chronic immune activation and aid the development of precise microbiota-targeted interventions to reverse or mitigate adverse outcomes.

即使持续使用抗逆转录病毒疗法 (ART)，HIV 感染者患全身性合并症和口腔病变的风险也会增加，包括机会性感染、口腔粘膜炎症以及牙龈和牙周病。在持续病毒抑制的情况下，导致这种风险增加的免疫介导机制尚不清楚。HIV 感染，即使得到控制，也会改变微生物群落，导致慢性低度炎症状态，这是这些非 HIV 合并症的基础。在接受 ART 治疗的 HIV 感染者中，龋齿、粘膜和牙周炎症的患病率较高，这通常与不同丰富的口腔微生物群落有关，这可能导致对炎症的易感性增加。这篇小型综述强调了当前关于微生物介导的口腔粘膜免疫与 HIV 感染相关的知识差距，同时讨论了未来研究调查的机会和实施新方法以阐明这些差距。需要针对炎症和微生物多样性的干预措施来减轻口腔炎症相关的合并症，特别是在 HIV 感染者中。更广泛地说，需要更多的研究来支持微生物组介导的慢性免疫激活的一般模型，并帮助开发针对微生物群的精确干预措施，以扭转或减轻不良后果。