Cellular protein HSC70 promotes fowl adenovirus serotype 4 replication in LMH cells via interacting with viral 100K protein.
Cellular protein HSC70 promotes fowl adenovirus serotype 4 replication in LMH cells via interacting with viral 100K protein.
复制标题
细胞蛋白HSC 70通过与病毒100K蛋白相互作用促进禽腺病毒血清4型在LMH细胞中的复制。
DOI：
10.1016/j.psj.2022.101941
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发表时间：
2022-07
期刊：
影响因子：
4.4
通讯作者：
Wang, Zeng
中科院分区：
文献类型：
--
作者：
Gao, Shenyan;Chen, Huayuan;Zhang, Xiaozhan;Zhao, Jun;Wang, Zeng
禽腺病毒血清4型（FAdV-4）是肝炎-心包积液综合征（HHS）的主要病原体，自2015年以来给养禽业造成了严重的经济损失。虽然纤维蛋白2和六邻体已被证实是FAdV-4致病性的相关因子，但病毒非结构蛋白在FAdV-4致病性中的作用仍知之甚少。本文采用串联质谱（MS）技术鉴定了与FAdV-4强毒分离株（CH/HNJZ/2015）100 K蛋白相互作用的宿主因子，并根据Gene Ontology和京都基因百科全书和基因组途径分析鉴定了2595个与多种生物学过程和途径相关的细胞蛋白。其中HSC 70蛋白通过免疫共沉淀实验证实能与100 K蛋白相互作用。值得注意的是，HSC 70的过表达促进了FAdV-4在LMH细胞中的复制，而用抑制剂ver-155008阻断HSC 70显著抑制了病毒复制。总之，这些发现表明，许多细胞蛋白通过与100 K和HSC 70相互作用参与FAdV-4感染，正调控病毒复制。
Fowl adenovirus serotype 4 (FAdV-4), the predominant causative agent of hepatitis-hydropericardium syndrome (HHS), has caused severe economic losses to poultry industry since 2015. Although fiber2 and hexon have been confirmed to be the virulence-related factors, the roles of nonstructural viral proteins in pathogenicity of FAdV-4 remain poorly understood. Here, a tandem mass spectrometry (MS) was used to identify host factors interacted with 100K protein of hypervirulent FAdV-4 isolate (CH/HNJZ/2015), and 2595 cellular proteins associated with many biological processes and pathways were identified according to Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses. Among the proteins, HSC70 was verified to interact with 100K through co-immunoprecipitation assay. Notably, overexpression of HSC70 promoted the replication of FAdV-4 in LMH cells, whereas blocking HSC70 with inhibitor ver-155008 markedly suppressed viral replication. Collectively, these findings suggested that many cellular proteins involved in FAdV-4 infection through interacting with 100K and HSC70 positively regulated virus replication.
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