研究证实HCV和HIV可在同一肝细胞内形成共感染，HIV Tat蛋白可以在淋巴细胞内诱导DDX3高表达，DDX3可与HCV Core蛋白结合促进HCV复制，而HIV Rev蛋白可与DDX3结合，在核膜上形成复合体从而降低胞浆内DDX3的水平。可以假设，HCV和HIV共感染形成后，HIV Tat诱导的DDX3高表达可促进HCV复制，而HIV Rev-DDX3复合体形成可竞争性的抑制这种促进作用。我们拟以自主构建的JFH-1全基因组复制子感染Huh-7.5细胞模型为研究对象，验证这一假设，阐明：①HIV Tat蛋白在Huh-7.5细胞内对DDX3表达调控的影响；②HIV Tat诱导Huh-7.5细胞DDX3高表达后对HCV复制的促进作用及关键机制；③DDX3-Rev-CRM-1复合体是否通过竞争的方式抑制DDX3-Core复合体的形成，从而减弱Tat对HCV复制的促进作用及其机制。

Previous studies have shown that HIV co-infected with HCV could be observed in one hepatocyte. Lately, some groups reported that HIV Tat could upregulate the expression of DDX3 in lymphocyntes while HIV Rev could reduce the DDX3 expression in cytoplasm via combining with DDX3. As a working hypothesis we have assumed that HIV Tat -induced DDX3 will accelerate the replication of HCV while HIV Rev-DDX3 complex will reduce HCV replication in HCV/HIV co-infected cells. To test this hypothesis, we focused our research on the following aspects by using JFH-1-infected-Huh-7.5 cells: exploring whether HIV Tat protein could upregulate the expression of DDX3 in JFH-1-infected-Huh-7.5 cells; probing whether HIV Tat-induced DDX3 could accelerate the replication of HCV in JFH-1-infected-Huh-7.5 cells and finding out its potential mechanisms; investigating whether DDX3-Rev-CRM-1 complex could resist the acceleration effect of HIV Tat on HCV replication by inhibiting the formation of DDX3-Core complex competitively and finally providing its underlying mechanisms.