PATHOGENESIS OF CARDIAC INJURY IN AIDS

艾滋病治疗的最新进展导致了长期的 生存率和更长的病程与多种新的临床 表现，包括心脏病的发病率增加 功能障碍尽管临床认识，艾滋病毒的发病机制， 心肌病是不清楚的，限制了应用这两个具体的 猴免疫缺陷病毒的治疗和预防策略 (SIV)导致猕猴患上一种类似艾滋病的疾病， 通过延长的临床潜伏期，弱中和抗体 应答、持续性病毒血症和骨髓源性 我们已经观察到左心室的生理证据， 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学， 在未感染的动物中没有发现这种SIV的最初特征 心肌病构成了第一个描述的实验性 艾滋病心功能不全的模型，并提供了一个独特的 因此，使用 SIV感染艾滋病猕猴模型，我们正在研究生理 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