PATHOGENESIS OF CARDIAC INJURY IN AIDS

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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