Elucidating the mechansim by which viruses manipulate cellular signalling pathways

为了使病毒成功感染，它必须利用宿主细胞机制进入细胞，启动病毒复制，并逃避宿主免疫反应。病毒已经进化出许多处理这些问题的方法，我的研究兴趣之一是了解病毒如何在分子水平上与宿主细胞相互作用。目前，我的研究重点是eb病毒（EBV）蛋白，潜伏膜蛋白2A （LMP2A）如何操纵细胞信号通路来影响细胞行为，以及最终如何使病毒受益。LMP2A含有许多短蛋白-蛋白相互作用基序，使其能够招募细胞信号蛋白。通过募集这些信号蛋白，LMP2A在某些情况下可以抑制宿主细胞信号通路，在其他情况下可以模拟宿主细胞信号通路。这对病毒至关重要，因为操纵细胞信号通路可以使EBV不被发现并在体内持续存在，并可能为EBV感染的细胞提供生存优势。我的目的是利用各种生化和分子技术，了解LMP2A如何操纵细胞信号通路，并改变细胞行为，使之有利于病毒。

In order for a virus to mount a successful infection, it must utilize the host-cell machinery to gain entry into the cell, initiate viral replication, and evade the host immune response.  Viruses have evolved a number of means of dealing with these problems, and one of my research interests is understanding how, at the molecular level, viruses interact with the host cell.  Currently, my focus is directed towards how the Epstein-Barr virus (EBV) protein, Latent Membrane Protein 2A (LMP2A), manipulates cellular signalling pathways to influence cellular behavior, and ultimately, how this benefits the virus. LMP2A contains a number of short protein-protein interaction motifs that enable it to recruit cellular signalling proteins.  Through recruiting these signalling proteins, LMP2A can in some cases inhibit, and in others mimic, host cell signalling pathways.  This is critically important for the virus, as manipulating cellular signalling pathways allows EBV to remain undetected and persist in the body and likely provides a survival advantage to the EBV-infected cell.  My aim is to understand, using a variety of biochemical and molecular techniques, how LMP2A manipulates cell signalling pathways and modifies cellular behavior to the advantage of the virus.