IMMUNOMORPHOLOGIC BASIS FOR SIV PATHOGENECITY

SIV 致病性的免疫形态学基础

• 批准号: 3454545
• 负责人: DOUGLAS J RINGLER
• 金额: $ 9.76万
• 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/3454545
• 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.

艾滋病（AIDS）是第一个 六年前的报告，发病率一直在无情地增加。 在对人类免疫缺陷病毒分子生物学的理解上取得了巨大的进步， 人类免疫缺陷病毒（HIV），病原体， 在这段时间内发生的，但致病的 导致各种形态学改变的机制 器官（例如脑、淋巴结、皮肤、胃肠道） 大部分未知。 这一空白的部分原因可能是 涉及的伦理、实践和流行病学考虑 确定和研究血清反应阳性的个人， 后来发展成艾滋病。 然而，这样的工作可能是 艾滋病的动物模型。 猴免疫缺陷病毒（SIV）是一种嗜T细胞慢病毒 与艾滋病病毒有着惊人的相似之处， 类似的免疫缺陷综合症。 工作 该提案中概述的目标是：1）确定 SIV感染，2）研究免疫形态学的时间顺序 感染期间淋巴器官的变化，以及3）与 这些发现与特定细胞的体外功能改变 表型 本工作所获得的结果可提供 对SIV和HIV发病机制的重要见解， 相关临床疾病。