CBFβ 受鲤鱼疱疹病毒春血症的诱导，并促进病毒在斑马鱼中的复制。
CBFβ is induced by spring viremia of carp virus and promotes virus replication in zebrafish.
机构信息
Key Laboratory of Exploration and Utilization of Aquatic Genetic Resources, Ministry of Education, Shanghai Ocean University, Shanghai, 201306, China; International Research Center for Marine Biosciences, Ministry of Science and Technology, Shanghai Ocean University, Shanghai, 201306, China; National Demonstration Center for Experimental Fisheries Science Education, Shanghai Ocean University, Shanghai, 201306, China.
Key Laboratory of Exploration and Utilization of Aquatic Genetic Resources, Ministry of Education, Shanghai Ocean University, Shanghai, 201306, China; International Research Center for Marine Biosciences, Ministry of Science and Technology, Shanghai Ocean University, Shanghai, 201306, China; National Demonstration Center for Experimental Fisheries Science Education, Shanghai Ocean University, Shanghai, 201306, China; Laboratory for Marine Biology and Biotechnology, Qingdao National Laboratory for Marine Science and Technology, Qingdao, 266200, China.
出版信息
Dev Comp Immunol. 2023 Oct;147:104751. doi: 10.1016/j.dci.2023.104751. Epub 2023 Jun 1.
The core binding factor subunit beta (CBFβ) is a transcription factor that forms a complex with virial proteins to promote viral infection. In this study, we identified a CBFβ homolog from zebrafish (zfCBFβ) and characterized the biological activity. The deduced zfCBFβ protein was highly similar to orthologs from other species. The zfcbfβ gene was constitutively expressed in tissues and was induced in immune tissues after infection with spring viremia carp virus (SVCV) and stimulation with poly(I:C). Interestingly, zfcbfβ is not induced by type I interferons. Overexpression of zfcbfβ induced tnfα expression but inhibited isg15 expression. Also, overexpression of zfcbfβ significantly increased SVCV titer in the EPC cells. Co-immunoprecipitation assay revealed that zfCBFβ interacts with SVCV phosphoprotein (SVCVP) and host p53, resulting in the increased stability of zfCBFβ. Our results provide evidence that CBFβ is targeted by virus to suppress host antiviral response.
核心结合因子亚基β（CBFβ）是一种转录因子，与病毒蛋白形成复合物，促进病毒感染。在这项研究中，我们从斑马鱼中鉴定出一个 CBFβ 同源物（zfCBFβ），并对其生物学活性进行了表征。推导的 zfCBFβ 蛋白与其他物种的同源物高度相似。zfcbfβ 基因在组织中持续表达，在感染春血病毒（SVCV）和用多聚（I：C）刺激后，在免疫组织中被诱导。有趣的是，zfCBFβ 不受 I 型干扰素的诱导。zfcbfβ 的过表达诱导了 tnfα 的表达，但抑制了 isg15 的表达。此外，zfcbfβ 的过表达显著增加了 EPC 细胞中的 SVCV 滴度。免疫共沉淀实验表明，zfCBFβ 与 SVCV 磷蛋白（SVCVP）和宿主 p53 相互作用，导致 zfCBFβ 的稳定性增加。我们的结果提供了证据表明，CBFβ 是病毒的靶标，以抑制宿主抗病毒反应。
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