HIV-2--A MODEL OF HIV PRIMARY INFECTION

HIV-2——HIV原发感染模型

• 批准号: 6170820
• 负责人: Phyllis J. Kanki
• 金额: $ 40.19万
• 依托单位: HARVARD SCHOOL OF PUBLIC HEALTH
• 依托单位国家: 美国
• 财政年份: 1998
• 资助国家: 美国
• 起止时间: 1998-09-01 至 2003-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6170820
• 关键词: African; HIV infections; cellular immunity; clinical research; cytotoxic T lymphocyte; epidemiology; female; high risk behavior /lifestyle; human immunodeficiency virus 1; human immunodeficiency virus 2; human subject; immunologic assay /test; pathologic process; prostitution; tissue /cell culture

DESCRIPTION (adapted from the Abstract): Studies of HIV2-infected individuals have demonstrated a significantly slower progression to AIDS. Most HIV-1 cohort studies have found 5-15% of their participants fit a definition of long-term non-progression, whereas 86-95% of HIV-2 infected individuals would be similarly classified. This dramatic difference in pathogenicity provides a unique opportunity to identify viral and host immune mechanisms involved in closely related and relevant virus system that is predicted to have a significantly slower course of progression. Significant advances in our understanding of HIV pathogenesis have come from studies of primary HIV-1 infection. The Principal Investigator proposes to characterize primary HIV-2 infection as a model system for long-term non-progressive HIV infection. The full spectrum of HIV primary infection will be assessed by recruiting women from a sub-selected high risk population, frequently monitored for early virologic and immunologic evidence of infection, irrespective of clinical symptomatology. By characterizing the cellular immune responses and viral characteristics found in primary HIV-2 infection, the Investigator believe that critical early determinants of HIV pathogenicity may be elucidated. She speculates that the lower pathogenicity of HIV-2 will be reflected in distinct difference sin the cellular immune responses to this virus during primary infection. Such responses would likely lower viral replication during this critical period of infection, resulting in a lowered viral set-point predictive of long progression. The identification of temporal, qualitative, and quantitative aspects of these immune responses should contribute to out growing understanding of the determinants of HIV pathogenicity.

描述（改编自摘要）：HIV 2感染者的研究 个体已经表现出明显更慢的进展为艾滋病。 大多数HIV-1队列研究发现，5-15%的参与者符合 长期非进展的定义，而86-95%的HIV-2感染者 个人也会被归类。这种巨大的差异， 致病性为鉴别病毒和宿主提供了独特的机会 与病毒系统密切相关的免疫机制 预计其进展会明显减慢。 我们对艾滋病发病机制的理解取得了重大进展， 从原发性HIV-1感染的研究中。主要研究者 建议将原发性HIV-2感染作为一个模型系统， 长期非进展性艾滋病毒感染。艾滋病病毒的主要传播途径 将通过从一个次级选定的高中招募妇女来评估感染情况， 危险人群，经常监测早期病毒学和免疫学 感染证据，无论临床表现如何。通过 表征细胞免疫应答和病毒特征 在原发性HIV-2感染中发现，研究者认为， 可以阐明HIV致病性的早期决定因素。她推测 HIV-2较低的致病性将反映在不同的 初级期间对该病毒的细胞免疫反应的差异 感染这样的反应可能会降低病毒在此期间的复制。 感染的关键时期，导致病毒设定点降低 预测长期进展。识别时间， 这些免疫应答的定性和定量方面应 促进我们对艾滋病毒决定因素的了解 致病性