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Fowl adenovirus serotype 4 52/55k protein triggers PKR degradation by ubiquitin-proteasome system to evade effective innate immunity

文献类型： 外文期刊

作者： He, Qing 1 ; Lu, Shaohua 1 ; Lin, Yun 1 ; Xu, Lihui 1 ; Chen, Zhen 3 ; Wang, Quanxi 1 ;

作者机构： 1.Fujian Agr & Forestry Univ, Fujian Key Lab Tradit Chinese Vet Med & Anim Hlth, Fuzhou 350002, Peoples R China

2.Univ Key Lab Integrated Chinese Tradit & Western V, Fuzhou 350002, Peoples R China

3.Fujian Acad Agr Sci, Inst Anim Husb & Vet Med, Fuzhou 350003, Peoples R China

4.Fujian Agr & Forestry Univ, Coll Anim Sci, Coll Bee Sci, Fuzhou 350002, Peoples R China

关键词： Fowl adenovirus serotype 4; 52; 55 K protein; Protein kinase R; Ubiquitin -proteasome system; Immune escape

期刊名称：VETERINARY MICROBIOLOGY （ 影响因子：3.3； 五年影响因子：3.5 ）

ISSN： 0378-1135

年卷期： 2023 年 278 卷

页码：

收录情况： SCI

摘要： The pro-and inflammatory cytokines fail to effectively inhibit FAdV-4, which has always puzzled us. In the current study, the data determined that the mRNA levels of interferons were significantly enhanced in the livers and LMH cells from 24 h to 72 h post FAdV-4 infection. But the viral load of FAdV-4 was still significantly increased, which meant that FAdV-4 evaded innate immune response. We additionally revealed that the protein levels not mRNA levels of PKR were degraded in host cell at 48 h post FAdV-4 infection. Moreover, the results of over expression and silent expression of PKR revealed that PKR could inhibit FAdV-4 proliferation. These results indicated that FAdV-4 degraded the protein levels of PKR to evade innate immune response. We also found that the protein degradation levels of PKR induced by FAdV-4 were recovery in LHM cells after treatment with proteasome inhibitor MG132, and ubiquitin-specific proteases inhibitor DUB-IN-1. Furthermore, our current data presented that FAdV-4 52/55 K protein directly interacted with PKR and degraded it determined by Co-immunoprecipitation and immunofluorescence. We also determined that 52/55 K protein triggered PKR degradation, and the degradation of PKR could be recovery in LHM cells after treatment with MG132, or DUB-IN -1, respectively. Finally, our data demonstrated that 52/55 K protein was a ubiquitylase that could directly degrade PKR protein in host cells via the ubiquitin-proteasome pathway. Therefore, the current study firstly revealed that FAdV-4 52/55 K protein played the key role in triggering PKR degradation by ubiquitin-proteasome system pathway to escape from innate immunity response.

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