Vpr作为HIV-1重要的辅助蛋白，可以利用宿主细胞NF-κB和AP-1信号通路激活HIV-1的复制。本研究拟从两条信号通路上游共同的信号蛋白TAK1入手，探索Vpr调节TAK1的分子机制，在此基础上探讨Vpr协同调节两条信号通路的模式，明确TAK1在Vpr活化NF-κB和AP-1信号通路中的作用，以期进一步阐明Vpr激活HIV-1的分子机理。同时为抗病毒药物新靶点的设计提供理论依据，也为揭示HIV-1感染过程中病毒与宿主细胞二者之间的相互关系提供新的数据。

Vpr, an accessory proteins of HIV-1, can activate the replication of HIV-1 through NF-κB and AP-1 signaling pathways. In this project, we focus on a common upstream signal protein TAK1 in these two signaling pathways and explore the molecular mechanism of Vpr in regulating TAK1. Based on these results, we will further investigate the mode how Vpr regulates the two signaling pathways and clarify the role of TAK1 in Vpr-mediated activation of NF-κB and AP-1 signaling pathway, in order to elucidate the molecular mechanism of Vpr in HIV-1 replication. These results can provide not only the theoretical basis for designing new antiviral drugs, but also important new data to reveal the interaction between HIV-1 and host cell.