Examination of the participation in HIV infection of the VitaminD3 and HSV-2 using the humanized mouse

疱疹单纯病毒（HSV）-2折叠与性感染艾滋病毒的增加风险有关。因为Langerhans细胞（LCs）被怀疑是艾滋病毒后续性暴露感染的初始目标细胞类型之一，我们评估了何时以及HSV-2对LCs的艾滋病毒感染有何影响。HSV-2刺激性表皮细胞的产生，包括人类、defensins和LL-37。培养表观细胞的宿主体内感染了HSV-2在mlCs中增强的艾滋病毒可疑性，这种影响被阻断LL-37生产暴露。这些数据提出了HSV-2增强艾滋病毒的性传播，增加了LCs通过外延细胞生产LL-37的艾滋病毒可疑性。

Herpes simplex virus (HSV)-2 shedding is associated with increased risk for sexually acquiring HIV. Because Langerhans cells (LCs)are suspected to be one of the initial target cell types infected by HIV following sexual exposure, we examined whether and how HSV-2 affects HIV infection of LCs. HSV-2 stimulated epithelial cell production of antimicrobial peptides (AMPs), including human ・ defensins and LL-37. Culture supernatants of epithelial cells infected with HSV-2 enhanced HIV susceptibility in mLCs, and this effect was abrogated by blocking LL-37 production. These data suggest that HSV-2 enhances sexual transmission of HIV by increasing HIV susceptibility of LCs via epithelial cell production of LL-37.