Determining Viral Pathogenesis in HIV SGD

确定 HIV SGD 的病毒发病机制

• 批准号: 6704372
• 负责人: Jennifer Y Webster-Cyriaque
• 金额: $ 1.68万
• 依托单位: UNIV OF NORTH CAROLINA CHAPEL HILL
• 依托单位国家: 美国
• 财政年份: 2003
• 资助国家: 美国
• 起止时间: 2003-02-10 至 2004-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6704372
• 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）近年来的工作一直针对 了解病毒在个体中的分子发病机制 免疫系统受损这项研究的长期目标是 了解病毒在口腔疾病中的分子发病机制， 在免疫功能低下的患者中发展。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， 在这些个体中引起显著的发病率。越来越多的发生在 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 并最终有针对性地实施适当的干预措施， 与HIV SGD相关的空洞发病率。核心假设是， 疱疹病毒因子对唾液腺的感染导致HIV SGD， 就像艾滋病淋巴瘤和卡波西肉瘤，这种病理学是一种直接的 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，使我们能够完善假设， 关于HIV SGD推定病原体的后续研究。目前还 这不是一个将临床疾病与病毒感染联系起来的好方法。一个主要 限制通常是试样的尺寸。这个小的最终目标 赠款提案旨在开发和验证新技术， 便于快速检测这些病原体及其感染状态， 他们的基因转录从最小的（和最少侵入性收集） 试样这些工具将使我们能够通过确定 HIV SGD中疱疹病毒存在、基因组结构和基因表达。