Cell-Type Specific Mechanisms of HIV Cardiomyopathy

项目摘要 到2030年，73%的艾滋病毒携带者将是50岁的≥，78%的人将患有心血管疾病。人民 携带艾滋病毒的人患急性心肌梗死的风险增加50%，患心力衰竭的风险增加61% 射血分数降低，心源性猝死率是一般人群的4倍 人口。除了传统的危险因素外，与艾滋病毒相关的特征，如慢性炎症和 在接受治疗的HIV感染的背景下，免疫失调是心血管疾病的强烈预测因素。 然而，阐明艾滋病毒心力衰竭发病机制的研究大多是描述性的，并已 因此，对这些疾病过程的潜在机制的洞察有限。因此，我们建议 通过研究HIV对免疫的影响来解决HIV感染者心力衰竭的发病机制 对构成人体心脏的多种细胞类型进行激活和抗逆转录病毒治疗。总的来说， 拟议的研究将阐明艾滋病毒心肌病的潜在机制，这可能被翻译为 创建针对艾滋病毒相关心脏病的细胞型特异性疗法。

Project Summary By 2030, 73% of people with HIV will be ≥ 50 years of age and 78% will have cardiovascular disease. People with HIV have a 50% increased risk of acute myocardial infarction, a 61% higher risk of heart failure with reduced ejection fraction and > 4 fold higher rates of sudden cardiac death compared to the general population. In addition to traditional risk factors, HIV-associated features such as chronic inflammation and immune dysregulation in the setting of treated HIV infection are strong predictors of cardiovascular disease. However, studies elucidating the pathogenesis of heart failure in HIV have been largely descriptive and have thus provided limited insight into the underlying mechanisms of these disease processes. Thus, we propose to address the pathogenesis of heart failure in people with HIV through investigating the impact of HIV, immune activation and antiretroviral therapies on the broad range of cell types comprising the human heart. Overall, the proposed studies will illuminate underlying mechanisms of HIV cardiomyopathy, which may be translated to the creation of cell-type specific therapies for HIV-related cardiac diseases.