HIV感染发病患者后期可出现严重的心血管并发症，极易造成患者心源性猝死，危害严重。以往研究认为抗HIV药物的应用很大程度上导致了其中致死性心律失常的发生，而对病毒来源致病原因认识甚少。本研究试图证明HIV心肌病及恶性心律失常发病过程中，HIV-1反式激活转录蛋白（Tat）可诱导心肌间质产生纤维化，并与细胞转化生长因子（TGF-β1）介导的Smads、Bax/Bcl-2等信号分子有关。尝试应用细胞共培养、膜片钳及分子生物学技术证明Tat蛋白通过促进成纤维细胞大量分泌TGF-β1，并旁分泌作用于心肌细胞HERG、Kir2.1、Cav1.2等通道产生异常调控，诱发心肌病并导致LQTs等恶性心律失常的发生。本课题的进行不但对HIV心肌病变的发病机制进行研究，完善对HIV-1 Tat蛋白功能的认识，同时将为临床抗HIV药物的应用提供指导依据。

Most of HIV infected patients are suffering the cardiovascular complications which usually cause sudden cardiac death. Some studies consider that the application of anti-HIV chemicals, especially protease inhibitors, induces lethal arrhythmia, but less of studies deem that the viral factors result in lethal arrhythmia. This project try to proof that HIV-1 Tat protein causes matrix cells fibrosis, consequence increases expression of TGF-β1 in procedure of HIV induced cardiomyopathy and lethal arrhythmia. Cells co-culture, patch clamping and molecular biological technique should be used to test if HIV-1 Tat protein effect the expression of HERG, Kir2.1 and Cav1.2 by increase expression of TGF-β1 and relative downstream pathway. By studying the pathogenesis of HIV induced cardiomyopathy, we can perfect the cognition of the function of HIV-1 Tat protein and instruct the management of anti-HIV medicines.