2. Academic Validation
  3. Getah virus Nsp3 binds G3BP to block formation of bona fide stress granules

Getah virus Nsp3 binds G3BP to block formation of bona fide stress granules

  • Int J Biol Macromol. 2024 Sep 1;279(Pt 2):135274. doi: 10.1016/j.ijbiomac.2024.135274.
Xiaoyi Qi 1,  Ruihan Zhao 1,  Xiaohui Yao 1,  Qinqiu Liu 1,  Panrao Liu 1,  Zhenbang Zhu 1,  Changchun Tu 2,  Wenjie Gong 3,  Xiangdong Li 4
Affiliations

Affiliations

  • 1 Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, College of Veterinary Medicine, Yangzhou University, Yangzhou 225009, China.
  • 2 Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, College of Veterinary Medicine, Yangzhou University, Yangzhou 225009, China; Changchun Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Changchun 130122, China.
  • 3 State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Key Laboratory for Zoonosis Research of the Ministry of Education, College of Veterinary Medicine, Jilin University, Changchun 130062, China.
  • 4 Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, College of Veterinary Medicine, Yangzhou University, Yangzhou 225009, China; Joint International Research Laboratory of Agriculture and Agri-Product Safety, The Ministry of Education of China, Yangzhou University, Yangzhou 225009, China. Electronic address: 007352@yzu.edu.cn.
PMID: 39226976 DOI: 10.1016/j.ijbiomac.2024.135274
Abstract

Stress granules (SGs) are cytoplasmic aggregates of proteins and mRNA that form in response to diverse environmental stressors, including viral infections. Several viruses possess the ability to block the formation of stress granules by targeting the SGs marker protein G3BP. However, the molecular functions and mechanisms underlying the regulation of SGs formation by Getah virus (GETV) remain unclear. In this study, we found that GETV Infection triggered the formation of Nsp3-G3BP aggregates, which differed in composition from SGs. Further studies revealed that the presence of these aggregates was dependent on the activation of the PKR/eIF2α signaling pathway. Interestingly, we found that Nsp3 HVD domain blocked the formation of SGs by binding to G3BP NTF2 domain. Moreover, knockout of G3BP in NCI-H1299 cells had no effect on GETV replication, while overexpression of G3BP to form the genuine SGs significantly inhibited GETV replication. Overall, our study elucidates a novel role GETV Nsp3 to change the composition of SG as well as cellular stress response.

Keywords

G3BP; GETV; Nsp3; Replication; Stress granules.

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