Figure 6 Emergence of opportunistic pathogens in the oral microbiome of ART naive HIV infected patients. (A) A statistically significant increase in the growth of Veillonella parvula was detected amongst all untreated HIV + subjects, while growth of (B) Campylobacter concisus/rectus, (C) Prevotella pallens, and (D) Megasphaera micronuciformis was significantly increased in untreated patients with HIV loads ≥ 50 K/mL of blood. Statistical analysis
was performed using Wilcoxon rank-sum tests. Discussion Maintenance Caspase inhibitor of oral health is dependent on preserving the homeostatic balance between host and the distinct microbial communities that colonize the various anatomical microenvironments in the oral cavity. HIV infected patients often display increased susceptibility to opportunistic oral infections GSK1210151A mouse that are presumably linked, in part, to disruption of host-microbe homeostasis (dysbiosis). In the current study, we utilize HOMIM-based analyses to characterize and compare the bacterial composition of the lingual microbiome in a relatively small, but well-defined cohort of untreated
chronically HIV infected patients (n = 6), HIV patients on ART (n = 6), and uninfected controls (n = 9). Due to the small sample sizes, it is important to caution that our ACP-196 cost findings represent a preliminary indication of the impact of HIV infection on the community structure of the oral microbiome. Indeed, the microbiome of even a single individual can be difficult to define, consisting of entrenched endogenous species and transient species whose prevalence can vary depending on time of sampling, diet, oral hygiene, and numerous
other parameters [19]. Extensive cross sectional and longitudinal sampling of patients with and without oral manifestations will ultimately be necessary to fully characterize the role of the microbiota in HIV associated oral pathogenesis. The current study represents an important first step towards that goal. Our findings indicate that chronic HIV infection may lead to substantial disruptions in the community structure of the lingual microbiota, even in the absence of clinical oral manifestations. Several potential mechanisms that have been revealed in previous studies may contribute to the development of host-microbe dysbiosis in the oral mucosa during Leukotriene-A4 hydrolase immunodeficiency virus infection. Recently, analysis of SIV infected rhesus macaques demonstrated that, similar to the gut mucosa, depletion of CD4+ T cells from the oral mucosa is rapid and dramatic [10]. This finding underscores the likelihood that immune dysfunction resulting from the loss of CD4+ T cell activity in the oral cavity could contribute to the development of oral manifestations during SIV/HIV infection. Recent studies suggest that Notch-1 signaling mediates epithelial barrier function in the gut through interaction with CD4+ T cells [25].