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

使用人源化小鼠检查维生素D3和HSV-2参与HIV感染的情况

• 批准号: 23659545
• 负责人: SHIMADA Shinji
• 金额: $ 2.41万
• 依托单位: University of Yamanashi
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Challenging Exploratory Research
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011 至 2012
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23659545/
• 关键词: HIV; HSV-2; 抗菌ペプチド; ランゲルハンス細胞; HIV感染; 性行為HIV感染; ＨＳＶ; ＨＩＶ; 経皮感染; 自然免疫

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.

单纯疱疹病毒（HSV）-2脱落与性感染HIV的风险增加有关。由于朗格汉斯细胞（LC）被怀疑是HIV感染后的性暴露的初始靶细胞类型之一，我们研究了HSV-2是否以及如何影响LC的HIV感染。HSV-2刺激上皮细胞产生抗菌肽（AMP），包括人防御素和LL-37。HSV-2感染的上皮细胞培养上清增强了mLC中的HIV易感性，并且通过阻断LL-37的产生来消除这种效应。这些数据表明HSV-2通过上皮细胞产生LL-37增加LC的HIV易感性来增强HIV的性传播。

项目成果

Antimicrobial Peptide LL-37 Produced by HSV-2-Infected Keratinocytes Enhances HIV Infection of Langerhans Cells

• DOI: 10.1016/j.chom.2012.12.002
• 发表时间: 2013-01-16
• 期刊: CELL HOST & MICROBE
• 影响因子: 30.3
• 作者: Ogawa, Youichi;Kawamura, Tatsuyoshi;Shimada, Shinji
• 通讯作者: Shimada, Shinji