白斑综合症病毒WSV083激酶促进对虾Tcf转录因子降解的分子机制研究

白斑综合症病毒（WSSV）是危害我国对虾养殖业的主要病原之一，目前对其仍无有效的防治手段。要解决这一病害问题，关键环节之一就是破解WSSV与宿主的互作机制，寻找病毒防治的潜在靶点。近年来研究证实，WSSV可通过多种方式“挟持”对虾免疫系统而促进自身复制。有趣的是，我们最近研究发现，WSSV蛋白激酶WSV083能够磷酸化对虾Tcf转录因子并促进其降解，这可能是WSSV调控宿主免疫的一种新的机制。然而，WSV083磷酸化Tcf的位点及其促进Tcf降解的分子机制等科学问题尚不清楚。为此，本项目拟进一步采用蛋白质组学、分子生物学和分子免疫学等技术，鉴定WSV083介导的与Tcf降解相关的磷酸化位点，揭示这些磷酸化位点调控Tcf降解的分子机制，探究WSV083促进Tcf降解对病毒增殖的影响。预期成果将有助于人们深入了解WSSV与宿主互作的分子机制，为WSSV的防治提供新的思路与科学依据。

White spot syndrome virus (WSSV) is one of the major lethal viruses of shrimp aquaculture, which currently has no effective control measures. Thus, it is crucial to explore the mechanisms of host-WSSV interactions to identify potential control targets of WSSV infection. Recent studies have found that WSSV adopts several strategies to hijack host immunity and to promote the expression of its own genes. Moreover, our recent study showed that WSV083, a viral serine/threonine-protein kinase, could phosphorylate the transcription factor Tcf to promote its degradation, which seems to be a novel mechanism used by WSSV to regulate host immunity. However, the phosphorylation sites of Tcf and the mechanism of its degradation triggered by WSV083 remain unknown. Here, further attempts will be made to identify the exact amino acid residue(s) on Tcf phosphorylated by WSV083, which relates to Tcf degradation. The molecular mechanisms of Tcf degradation via regulation of these phosphorylation sites and the effect on WSSV proliferation would also be examined. This proposed project will contribute to an in-depth understanding of host-WSSV interaction and provide new theoretical ideas for the control of WSSV infection.