中国农业科技导报 ›› 2023, Vol. 25 ›› Issue (9): 131-139.DOI: 10.13304/j.nykjdb.2022.0538

• 动植物健康 • 上一篇    下一篇

疱疹病毒引起内质网应激/未折叠蛋白反应研究进展

蔡海情1(), 王微1, 曾茂芹1, 毕文文1, 陈莉1, 张黔东1, 袁阳1, 文明1,2()   

  1. 1.贵州大学动物科学学院,贵阳 550025
    2.贵州省动物生物制品工程技术研究中心,贵阳 550025
  • 收稿日期:2022-06-28 接受日期:2023-01-03 出版日期:2023-09-15 发布日期:2023-09-28
  • 通讯作者: 文明
  • 作者简介:蔡海情 E-mail:2178506814@qq.com
  • 基金资助:
    国家自然科学基金项目(31560703)

Research Progress on Endoplasmic Reticulum Stress/Unfolded Protein Response Caused by Herpesvirus

Haiqing CAI1(), Wei WANG1, Maoqin ZENG1, Wenwen BI1, Li CHEN1, Qiandong ZHANG1, Yang YUAN1, Ming WEN1,2()   

  1. 1.College of Animal Science,Guizhou University,Guiyang 550025,China
    2.Guizhou Provincial Animal Biological Products Engineering Technology Research Center,Guiyang 550025,China
  • Received:2022-06-28 Accepted:2023-01-03 Online:2023-09-15 Published:2023-09-28
  • Contact: Ming WEN

摘要:

内质网是真核细胞内蛋白质折叠及翻译后修饰的主要场所,还参与调控Ca2+和脂类物质储存合成,具有重要生理功能。疱疹病毒是一类具有囊膜的DNA病毒,其表面糖基化囊膜蛋白的合成加工依赖于内质网,在病毒复制过程中,大量合成的糖基化囊膜蛋白在内质网内过度堆积则会引起内质网应激(endoplasmic reticulum stress,ERS),进而发生未折叠蛋白反应(unfolded protein response,UPR)。某些疱疹病毒可能已经进化出调控UPR的机制,为复制过程创造最佳环境,它们在宿主细胞内复制时,会引起相关内质网UPR信号级联反应,如细胞损伤、炎症反应、细胞凋亡等。综述了内质网应激/未折叠蛋白(ERS/UPR)对病毒的反应机制,从Ⅰ型单纯疱疹病毒、伪狂犬病病毒、马立克病病毒、鸭肠炎病毒和其他疱疹病毒等感染引起ERS分子机制及相关信号通路进行阐述,以期为疱疹病毒相关疫苗和药物作用靶点的研发提供理论依据。

关键词: 内质网应激, 未折叠蛋白反应, 疱疹病毒

Abstract:

Endoplasmic reticulum is the main site of protein folding and post-translational modification in eukaryotic cells. It also participates in the regulation of Ca2+ and lipid storage and synthesis, and has important physiological functions. Herpesviruses is a class of enveloped DNA viruses. The synthesis and processing of its surface glycosylated envelope proteins depends on the endoplasmic reticulum. During virus replication, a large number of synthesized glycosylated envelope proteins are excessive in the endoplasmic reticulum. Accumulation causes endoplasmic reticulum stress (ERS), which in turn leads to unfolded protein response (UPR). Some herpesviruses may have evolved mechanisms to regulate the UPR to create an optimal egoistic environment for the replication process. When they replicate in host cells, they will cause related endoplasmic reticulum UPR signaling cascades, such as cell damage, inflammation, apoptosis, etc. In this paper, the mechanism of endoplasmic reticulum stress/unfolded protein response (ERS/UPR) response to viruses was reviewed, and the molecular mechanism and related signaling pathways of ERS caused by herpes simplex virus type Ⅰ, pseudorabies virus, marek virus, duck enteritis virus and other herpes viruses were expounded, which provided theoretical basis for the research and development of herpes virus-related vaccines and drug targets.

Key words: endoplasmic reticulum stress, unfolded protein response, herpesvirus

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