Litopenaeus vannamei Src64B restricts white spot syndrome virus replication by modulating apoptosis
Litopenaeus vannamei Src64B restricts white spot syndrome virus replication by modulating apoptosis
复制标题
凡纳滨对虾 Src64B 通过调节细胞凋亡来限制白斑综合症病毒复制
DOI：
10.1016/j.fsi.2019.07.062
复制
发表时间：
2019
影响因子：
4.7
通讯作者：
Yao Defu
中科院分区：
文献类型：
--
作者：
Wei Menghao;Zhang Yueling;Aweya Jude Juventus;Wang Fan;Li Shengkang;Lun Jingsheng;Zhu Chunhua;Yao Defu
Src 家族激酶 (SFK) 参与调节多种生物活性（包括宿主与病毒相互作用）的信号转导。 SFK 的这些特征已在脊椎动物中得到了很好的探索，然而，在虾中，无脊椎动物 SFK 家族成员 Src64B 尚未得到表征，因此其在虾-病毒相互作用中的作用仍然未知。在本研究中，首先克隆了两种凡纳滨对虾 Src64B 亚型（命名为 LvSrc64B1 和 LvSrc64B2），并探讨了它们在白斑综合症病毒（WSSV）感染中的作用。生物信息学分析显示，LvSrc64B1和LvSrc64B2与其他Src64B家族成员相似，一级和三级结构具有高度同源性，并含有保守的SFK功能域以及推定的肉豆蔻酰化和磷酸化位点。组织分布分析表明，两种 LvSrc64B 亚型均普遍表达，尽管在测试组织中表达不同。此外，LvSrc64B1 和 LvSrc64B2 的转录水平在 WSSV 攻击后显着诱导，并且具有相似的表达模式。此外，WSSV 感染后 siRNA 介导的 LvSrc64B1 和 LvSrc64B2 敲低导致病毒基因表达增加、病毒 DNA 复制增强和血细胞凋亡增加。 LvSrc64B1 和 LvSrc64B2 的耗尽也会降低 WSSV 感染后虾的存活率。总之，目前的数据强烈表明 Src64B 是一种宿主因子，通过调节虾的细胞凋亡来抑制 WSSV 复制。
The Src family kinases (SFK) are involved in signaling transductions that regulate numerous biological activities including host-virus interaction. These features of SFK have been well explored in vertebrates, however, in shrimp, the invertebrate SFK family member Src64B, has not been characterized and therefore its role in shrimp-virus interaction remains unknown. In this study, two Litopenaeus vannamei Src64B isoforms (designated LvSrc64B1 and LvSrc64B2) were first cloned and their role in white spot syndrome virus (WSSV) infection was explored. Bioinformatics analysis revealed that LvSrc64B1 and LvSrc64B2 were similar to other Src64B family members, with high homology in primary and tertiary structures, and contained the conserved SFK functional domains, as well as the putative myristylation and phosphorylation sites. Tissue distribution analysis showed that both LvSrc64B isoforms were ubiquitously expressed, albeit distinctively in the tested tissues. In addition, transcript levels of LvSrc64B1 and LvSrc64B2 were significantly induced following WSSV challenge and had similar expression patterns. Furthermore, siRNA-mediated knockdown of LvSrc64B1 and LvSrc64B2 followed by WSSV infection resulted in increased expression of viral genes, enhanced viral DNA replication, and elevation of hemocytes apoptosis. Depletion of LvSrc64B1 and LvSrc64B2 also reduced shrimp survival upon WSSV infection. In conclusion, the current data strongly suggest that Src64B is a host factor that inhibits WSSV replication by modulating apoptosis in shrimp.