PATHOGENESIS OF CARDIAC INJURY IN AIDS

最近在艾滋病治疗方面的进展导致了 多个新临床病例的存活率和更长的病程 表现，包括心脏病发病率的增加 尽管临床认识到功能障碍，但艾滋病毒的发病机制 心肌病尚不清楚，限制了两者的具体应用 猿猴免疫缺陷病毒的治疗与预防策略 (SIV)在猕猴身上引起一种类似艾滋病的疾病，其特征通常是 通过延长临床潜伏期，一种弱中和抗体 骨髓来源的应答、持续性病毒血症和嗜性 细胞我们观察到了左心室的生理学证据 扩张和收缩功能障碍以及相关的 SIV感染恒河猴的心肌和血管病理 在未感染的动物身上看不到这种SIV的最初特征 心肌病构成了实验性心肌病的第一个描述 艾滋病心功能不全模型为S提供了独特的 因此，有机会研究其发病机制，使用 感染SIV的恒河猴艾滋病模型，我们正在检查生理 和艾滋病相关心肌病的细胞基础

Recent progress in the treatment of AIDS has resulted in prolonged survival and a more protracted course with multiple new clinical manifestations, including an increasing incidence of cardiac dysfunction Despite the clinical recognition, the pathogenesis of HIV cardiomyopathy is unclear, limiting the application of both specific treatments and preventive strategies Simian immunodeficiency virus (SIV) causes an AIDS-like illness in macaques generally characterized by a prolonged clinical latency, a weak neutralizing antibody response, persistent viremia, and tropism for bone marrow-derived cells We have observed physiological evidence of left ventricular dilatation and contractile dysfunction, as well as associated myocardial and vascular pathology in SIV-infected rhesus monkeys which is not seen in uninfected animals This initial characterization of SIV cardiomyopathy constitutes the first description of an experimental model of cardiac dysfunction in AIDS a nd afford s a unique opportunity to investigate its pathogenesis Therefore, using the SIV-infected macaque model of AIDS, we are examining the physiological and cellular basis of AIDS-associated cardiomyopathy