AIDS相关卡波氏肉瘤（AIDS-KS）发病后预后差、病死率高。卡波氏肉瘤病毒（KSHV）感染并非KS发生的充分条件，HIV-1这一重要协同因子在KS致病中发挥着重要作用。我们前期的研究表明，HIV-1 Tat通过调控STAT3和PI3K/AKT等信号通路加速KSHV Kaposin A致瘤（Neoplasia, 2009, 11: 1272）。那么，Tat是否有可能通过某种机制来促进KSHV另一个致瘤蛋白病毒白细胞介素6（vIL-6）诱导血管生成和肿瘤形成？.本研究的目的是证实Tat能够促进KSHV vIL-6诱导血管生成和肿瘤形成；鉴定调控上述促进过程的关键信号通路；寻找调控上述促进过程的重要miRNAs，并阐明其作用机制。.本研究有助于进一步认识HIV-1与KSHV分子之间的相互作用，阐明AIDS-KS发病的分子机制，为从信号通路和miRNA角度辅助治疗AIDS-KS提供理论依据。

The prognosis of AIDS-KS is poor and the mortality of AIDS-KS is high. The infection of Kaposi's sarcoma-associated herpesvirus (KSHV) is not enough for KS occurrence. The important cofactor HIV-1 plays an important role in KS pathogenesis. We have previous showed that HIV-1 Tat accelerated Kaposin A-induced tumorigenesis by regulating STAT3 and PI3K/AKT signaling pathways (Neoplasia, 2009, 11: 1272). Therefore, the working hypothesis of this project is that HIV-1 Tat can promote KSHV viral interleukin-6 (vIL-6)-mediated angiogenesis and tumorigenesis by some mechanisms. .To test this hypothesis, we will perform the following specific aims: (1) To confirm that HIV-1 Tat can facilitate KSHV vIL-6-induced angiogenesis and tumorigenesis; (2) To identify the key signaling pathways and important miRNAs, which regulate HIV-1 Tat to promote vIL-6-induced angiogenesis and tumorigenesis..This study will help to further understand the interaction between HIV-1 and KSHV, to clarify the molecular mechanism of AIDS-KS pathogenesis, and provide the theoretical basis for the treatment of AIDS-KS from the perspective of signal pathway and miRNAs.