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Chicken Eef1 Alpha Is A Critical Factor For The Polymerase Complex Activity Of Very Virulent Infectious Bursal Disease Virus

文献类型： 外文期刊

作者： Yang, B; Yan, NN; Liu, AJ; Li, Y; Chen, ZH; Gao, L; Qi, XL; Gao, YL; Liu, CJ; Zhang, YP; Cui, HY; Li, K; Pan, Q; Wang, YQ; Wang, XM

作者机构：

关键词： Vvibdv; Eef1 Alpha; Vp3; Polymerase

期刊名称： VIRUSES-BASEL

ISSN： 19994915

年卷期： 2020 年 12 卷 2 期

页码：

收录情况： JCR（2021版）

摘要： Infectious bursal disease (IBD) is an immunosuppressive, highly contagious, and lethal disease of young chickens caused by IBD virus (IBDV). It results in huge economic loss to the poultry industry worldwide. Infection caused by very virulent IBDV (vvIBDV) strains results in high mortality in young chicken flocks. However, the replication characteristics of vvIBDV are not well studied. Publications have shown that virus protein 3 (VP3) binds to VP1 and viral double-stranded RNA, and together they form a ribonucleoprotein complex that plays a key role in virus replication. In this study, vvIBDV VP3 was used to identify host proteins potentially involved in modulating vvIBDV replication. Chicken eukaryotic translation elongation factor 1 alpha (cheEF1 alpha) was chosen to further investigate effects on vvIBDV replication. By small interfering RNA-mediated cheEF1 alpha knockdown, we demonstrated the possibility of significantly reducing viral polymerase activity, with a subsequent reduction in virus yields. Conversely, over-expression of cheEF1 alpha significantly increased viral polymerase activity and virus replication. Further study confirmed that cheEF1 alpha interacted only with vvIBDV VP3 but not with attenuated IBDV (aIBDV) VP3. Furthermore, the amino acids at the N- and C-termini were important in the interaction between vvIBDV VP3 and cheEF1 alpha. Domain III was essential for interactions between cheEF1 alpha and vvIBDV VP3. In summary, cheEF1 alpha enhances vvIBDV replication by promoting the activity of virus polymerase. Our study indicates cheEF1 alpha is a potential target for limiting vvIBDV infection.

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