Inflammatory and Immune Mechanisms of Atherosclerosis in HIV-Infected Women

描述（由申请人提供）： 这项研究将检查免疫，炎症，凝血和脂质紊乱作为增加动脉粥样硬化的HIV感染的妇女参与妇女的机构间HIV研究（WIHS）的潜在介质。受试者将包括750名HIV感染和250名HIV未感染的女性，参与WIHS颈动脉超声研究的随访期。这组具体目标包括两个主要目标：目标1侧重于确定炎症和凝血生物标志物作为亚临床动脉粥样硬化的预测因子。目的2：研究构成“经典”血管危险因素的血脂变化。数据分析的目标是：（1）将炎症和凝血标志物的变化与HIV疾病分期和治疗相关联，包括HAART的开始以及病毒血症和CD 4+状态的变化;（2）确定免疫、炎症和凝血机制是否有助于HIV感染女性中动脉粥样硬化的增加;（3）确定“经典”血管危险因素（例如，脂质）随着时间的推移，由于HAART和HIV疾病阶段的变化，以及这如何影响动脉粥样硬化。此外，我们提出了三个探索性的目标，检查新的免疫和炎症介质，可能是重要的动脉粥样硬化在艾滋病毒感染的成年人：1。肠道微生物的易位，通过16 s RNA测量; 2. T细胞衰老（CD 4 + CD 28-T细胞和CD 8 + CD 28-T细胞）; 3.调节性T细胞这项研究将检查免疫，炎症，凝血和脂质紊乱作为增加动脉粥样硬化的HIV感染的妇女参与妇女的机构间HIV研究（WIHS）的潜在介质。我们将（1）将炎症和凝血标志物的变化与HIV疾病分期和治疗相关联，包括HAART的启动以及病毒血症和CD 4+状态的变化;（2）确定免疫、炎症和凝血机制是否有助于HIV感染女性动脉粥样硬化的增加;（3）确定“经典”血管危险因素的变化（例如，脂质）随着时间的推移，由于HAART和HIV疾病阶段的变化，以及这如何影响动脉粥样硬化。(End摘要）

DESCRIPTION (provided by applicant): This investigation will examine immune, inflammatory, coagulation, and lipid disturbances as potential mediators of increased atherosclerosis in HIV-infected women participating in the Women's Interagency HIV Study (WIHS). Subjects will include 750 HIV-infected and 250 HIV-uninfected women participating in the Follow-up Phase of the WIHS Carotid Artery Ultrasound Study. The set of specific aims include two primary aims: Aim 1 focuses on established inflammation and coagulation biomarkers as predictors of subclinical atherosclerosis. Aim 2 examines lipid changes which constitute "classic" vascular risk factors. Data analysis goals are: (1) To correlate changes in inflammatory and coagulation markers with HIV disease stage and treatments, including initiation of HAART and changes in viremic and CD4+ status; (2) To determine if immune, inflammatory, and coagulation mechanisms contribute to increased atherosclerosis in HIV-infected women; (3) To determine changes in "classic" vascular risk factors (e.g., lipids) over time due to changes in HAART and HIV disease stage, and how this impacts atherosclerosis. In addition, we propose three exploratory aims examining novel immune and inflammatory mediators that may be of importance to atherosclerosis in HIV-infected adults: 1. Translocation of gut microbes, as measured by 16s RNA; 2. T-cell senescence (CD4+CD28- and CD8+CD28- T-cells); 3. T regulatory cells. This investigation will examine immune, inflammatory, coagulation, and lipid disturbances as potential mediators of increased atherosclerosis in HIV-infected women participating in the Women's Interagency HIV Study (WIHS). We will (1) correlate changes in inflammatory and coagulation markers with HIV disease stage and treatments, including initiation of HAART and changes in viremic and CD4+ status; (2) determine if immune, inflammatory, and coagulation mechanisms contribute to increased atherosclerosis in HIV-infected women; and (3) determine changes in "classic" vascular risk factors (e.g., lipids) over time due to changes in HAART and HIV disease stage, and how this impacts atherosclerosis. (End of Abstract)