HIV-2--A MODEL OF HIV PRIMARY INFECTION

描述(摘自摘要)：HIV2感染的研究 个人患上艾滋病的速度要慢得多。 大多数HIV-1队列研究发现，5%-15%的参与者符合 长期无进展的定义，而86-95%的艾滋病毒-2感染者 个人也会被类似地归类。这一戏剧性的差异 致病性为识别病毒和宿主提供了一个独特的机会 密切相关的病毒系统涉及的免疫机制 据预测，这一过程的进展要慢得多。 我们对艾滋病毒发病机制的了解取得了重大进展 来自对HIV-1原发感染的研究。首席调查员 建议将原发HIV-2感染定性为 长期非进行性艾滋病毒感染。全谱的HIV原发病例 感染评估将通过招募女性从一所分选的高中进行 危险人群，经常监测早期病毒学和免疫学 感染的证据，与临床症状无关。通过 细胞免疫反应和病毒特征的特征 在最初的HIV-2感染中发现，调查人员认为关键 HIV致病性的早期决定因素可能会被阐明。她推测 HIV-2的低致病性将在不同的 初选期间对该病毒的细胞免疫应答的差异 感染。在此期间，这种反应可能会降低病毒复制 感染的关键时期，导致病毒设定点降低 预示着长期的进步。对时间的识别， 这些免疫反应的定性和定量方面应该 有助于加深对艾滋病毒决定因素的了解 致病性。

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.