MECHANISMS OF ORAL SIV TRANSMISSION

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 为了测试青少年口腔粘膜炎症是否促进了口腔接触后的病毒传播，我们建立了一个暂时性口腔炎症的灵长类动物模型。我们使用局部注射10%的醋酸(HAC)到麻醉猴子的右脸颊粘膜下层来诱导口腔炎症；这一程序在仓鼠身上已经很好地建立了(J.药用植物。SCI。3(1)：114-117,2000)。我们确定了恒河猴产生炎症而几乎没有轻度溃疡所需的剂量。我们的数据显示，与对照组相比，在口腔炎症存在的情况下，幼年恒河猴的SIV-1157ipd3N4口腔传播显著增加。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. In order to test whether inflammation of the oral mucosa in juveniles facilitates virus transmission after oral exposure, we established a primate model for transient oral inflammation. We used local injection of 10% acetic acid (HAc) into the submucosa of the right cheek of anesthetized monkeys to induce inflammation in the mouth; this procedure has been well established in hamsters (J. Pharm. Pharmaceut. Sci. 3(1):114-117, 2000). We determined the dose needed in rhesus macaques to generate an inflammation with few mild ulcers. Our data showed a significant increase of oral SHIV-1157ipd3N4 transmission in the presence of oral inflammation in juvenile rhesus macaques compared to controls.