IMMUNOMORPHOLOGIC BASIS FOR SIV PATHOGENECITY

SIV 致病性的免疫形态学基础

• 批准号: 3454548
• 负责人: DOUGLAS J RINGLER
• 金额: $ 9.36万
• 依托单位: HARVARD MEDICAL SCHOOL
• 依托单位国家: 美国
• 财政年份: 1988
• 资助国家: 美国
• 起止时间: 1988-02-01 至 1993-01-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3454548
• 关键词: AIDS; Langerhans' cell; Macaca mulatta; antigen presentation; cell population study; cellular pathology; gene expression; histochemistry /cytochemistry; histocompatibility antigens; human immunodeficiency virus 1; immunochemistry; immunoelectron microscopy; immunogenetics; immunosuppression; inflammation; interleukin 2; mixed tissue /cell culture; model design /development; monoclonal antibody; nucleic acid hybridization; receptor; simian AIDSs; simian immunodeficiency virus; skin disorder; virus cytopathogenic effect; virus infection mechanism

Since Acquired Immunodeficiency Syndrome (AIDS) was first reported six years ago, the incidence has relentlessly increased. Great advances in the understanding of the molecular biology of human immunodeficiency virus (HIV), the etiologic agent, have occurred during this time period, but the pathogenetic mechanisms leading to the morphologic alterations in various organs (e.g. brain, lymph node, skin, gastrointestinal tract) are largely unknown. Part of this void may be explained by the ethical, practical and epidemiological considerations involved in identifying and studying seropositive individuals who will subsequently develop AIDS. Such work, however, could be facilitated with an animal model for AIDS. Simian immunodeficiency virus (SIV) is a T-cell tropic lentivirus with remarkable parallels to HIV, and it induces a strikingly similar immunodeficiency syndrome in rhesus monkeys. The work outlined in this proposal seeks to 1) identify cellular targets of SIV-infection, 2) study the chronological immunomorphologic changes in lymphoid organs during infection, and 3) correlate these findings with in vitro functional alterations of specific cell phenotypes. The results obtained by this work may provide important insights into the pathogenesis of both SIV- and HIV- related clinical disease.

自从获得性免疫缺陷综合症（艾滋病）首次出现以来 据报道，六年前，发病率不断增加。 对分子生物学的理解取得了巨大进步 人类免疫缺陷病毒（HIV）作为病原体， 发生在这个时期，但发病原因 导致各种形态改变的机制 器官（例如脑、淋巴结、皮肤、胃肠道） 很大程度上不为人知。 这种空白的部分原因可能是 涉及伦理、实践和流行病学方面的考虑 识别和研究血清反应呈阳性的个体 随后发展为艾滋病。 然而，这样的工作可能是 艾滋病动物模型促进了这一过程。 猿猴免疫缺陷病毒 (SIV) 是一种 T 细胞嗜性慢病毒 与艾滋病毒有显着的相似之处，并且它引起了惊人的 恒河猴也有类似的免疫缺陷综合症。 工作 该提案中概述的目的是 1) 确定细胞目标 SIV 感染，2) 按时间顺序研究免疫形态学 感染期间淋巴器官的变化，以及 3) 相关 这些发现与特定细胞的体外功能改变有关 表型。 这项工作获得的结果可能会提供 对 SIV 和 HIV 发病机制的重要见解 相关临床疾病。