Determining Viral Pathogenesis in HIV SGD

确定 HIV SGD 的病毒发病机制

• 批准号: 6793904
• 负责人: Jennifer Y Webster-Cyriaque
• 金额: $ 3.27万
• 依托单位: UNIV OF NORTH CAROLINA CHAPEL HILL
• 依托单位国家: 美国
• 财政年份: 2002
• 资助国家: 美国
• 起止时间: 2002-08-01 至 2004-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6793904
• 关键词: AIDS related neoplasm /cancer; Epstein Barr virus; HIV infections; Herpesviridae disease; Kaposi's sarcoma; RNA; clinical research; complementary DNA; cytomegalovirus; disease /disorder etiology; gene expression; genetic markers; high throughput technology; human tissue; immunocytochemistry; microarray technology; polymerase chain reaction; salivary disorder; tissue /cell culture; virus cytopathogenic effect; virus infection mechanism; virus protein

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.

描述：（由申请人提供）近年来的工作已针对 了解个体病毒分子发病机理的机制 与免疫系统受损。这项研究的远程目标是 了解口腔疾病中病毒分子发病机理的机制 在免疫功能低下的患者中发育。艾滋病相关的恶性肿瘤包括 Kaposi的肉瘤和相关淋巴瘤是疱疹病毒相关的 在这些个体中引起明显的发病率。越来越多的发生率 艾滋病毒相关的唾液腺疾病（HIV SGD），一种前病变， 提供了阐明这种口腔感染的发病机理的机会 最终针对并实施适当的干预措施以减少口服 与HIV SGD相关的空腔发病率。中心假设是 用疱疹病毒剂感染唾液腺导致HIV SGD， 就像AIDS淋巴瘤和Kaposi的肉瘤一样，这种病理是一种直接的 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 随后有关HIV SGD假定病原体的研究。目前有 将临床疾病与病毒感染联系起来不是一个好方法。专业 限制通常是标本的大小。这个小的目标的最终目标 赠款提案是开发和验证可以 促进这些病原体的快速检测，它们的感染状态和 它们的基因转录来自最小的（最少侵入性收获） 标本。这些工具将使我们通过确定来完善我们的假设 HIV SGD中的疱疹病毒存在，基因组结构和基因表达。