Determining Viral Pathogenesis in HIV SGD

描述：(申请人提供)近年来的工作针对的是 了解病毒在个体中的分子致病机制 免疫系统受损。这项研究的长期目标是 了解口腔疾病中病毒分子致病机制 发生在免疫功能低下的患者身上。与艾滋病相关的恶性肿瘤包括 卡波西肉瘤和艾滋病相关淋巴瘤是疱疹病毒相关的 在这些人中造成严重的发病率。……的发病率不断增加 HIV相关唾液腺疾病(HIV SGD)，一种癌前病变， 为阐明这种口腔感染的发病机制提供了机会。 并最终针对并实施适当的干预措施以减少口腔 与HIV SGD相关的空洞发病率。中心假设是 用疱疹病毒制剂感染唾液腺会导致HIV SGD， 就像艾滋病淋巴瘤和卡波西肉瘤一样，这种病理是直接的 疱疹病毒病原体调节细胞环境的结果。这 假设生成提案寻求资金，以使我们能够完善假设 关于HIV、SGD推定病原体的后续研究。目前有 不是将临床疾病与病毒感染联系起来的好方法。一位少校 限制通常是样本的大小。这一小型项目的最终目标是 资助计划旨在开发和验证能够 促进快速检测这些病原体及其感染状态，以及 他们的基因转录从最小的(和最不具侵入性的收集) 样本。这些工具将允许我们通过确定 HIV SGD中疱疹病毒的存在、基因组结构和基因表达。

DESCRIPTION: (provided by applicant) Work in recent years has been directed to understanding the mechanisms of viral molecular pathogenesis in individuals with compromised immune systems. The long-range goal of this research is to understand mechanisms of viral molecular pathogenesis in oral disease that develops in immunocompromised patients. AIDS associated malignancies including Kaposi's Sarcoma and AIDS associated lymphoma are herpes virus associated and cause significant morbidity in these individuals. An increasing incidence in HIV-associated salivary gland disease (HIV SGD), a premalignant lesion, provides an opportunity to elucidate the pathogenesis of this oral infection and eventually target and implement appropriate interventions to decrease oral cavity morbidity associated with HIV SGD. The central hypothesis is that infection of the salivary glands with herpesviral agents results in HIV SGD, and that like AIDS lymphoma and Kaposi's Sarcoma, this pathology is a direct result of modulation of the cellular environment by herpesviral pathogens. This hypothesis-generating proposal seeks funds to allow us to refine hypotheses for subsequent studies regarding HIV SGD putative pathogens. At present there is not a good method for linking clinical disease to viral infection. A major limitation is often the size of the specimen. The ultimate goals of this small grant proposal are to develop and validate novel technologies that can facilitate rapid detection of these pathogens, their state of infection, and their gene transcription from the smallest (and least invasively-collected) specimen. These tools will allow us to the refine our hypothesis by determining herpesviral presence, genomic structure, and gene expression in HIV SGD.