2. Academic Validation
  3. Encephalomyocarditis virus non-structural protein 2C induces the degradation of NDP52 autophagy protein to promote its own survival

Encephalomyocarditis virus non-structural protein 2C induces the degradation of NDP52 autophagy protein to promote its own survival

  • Vet Microbiol. 2025 Jul:306:110549. doi: 10.1016/j.vetmic.2025.110549.
Rongqian Mo 1,  Rongrong Cheng 2,  Pingan Dong 2,  Tingting Ma 2,  Yaxin Zhang 2,  Jingying Xie 2,  Shasha Li 2,  Huixia Li 2,  Adi Idris 3,  Xiangrong Li 4,  Ruofei Feng 5
Affiliations

Affiliations

  • 1 Engineering Research Center of Key Technology and Industrialization of Cell-based Vaccine, Ministry of Education, Biomedical Research Center, Northwest Minzu University, Lanzhou 730030, China; Gansu Tech Innovation Center of Animal Cell, Biomedical Research Center, Northwest Minzu University, Lanzhou 730030, China; Key Laboratory of Biotechnology and Bioengineering of State Ethnic Affairs Commission, Biomedical Research Center, Northwest Minzu University, Lanzhou 730030, China; School of Life Sciences and Engineering, Northwest Minzu University, Lanzhou 730030, China.
  • 2 Engineering Research Center of Key Technology and Industrialization of Cell-based Vaccine, Ministry of Education, Biomedical Research Center, Northwest Minzu University, Lanzhou 730030, China; Key Laboratory of Biotechnology and Bioengineering of State Ethnic Affairs Commission, Biomedical Research Center, Northwest Minzu University, Lanzhou 730030, China; School of Life Sciences and Engineering, Northwest Minzu University, Lanzhou 730030, China.
  • 3 Centre for Immunology and Infection Control, School of Biomedical Sciences, Queensland University of Technology, Kelvin Grove, Queensland 4702, Australia.
  • 4 Engineering Research Center of Key Technology and Industrialization of Cell-based Vaccine, Ministry of Education, Biomedical Research Center, Northwest Minzu University, Lanzhou 730030, China; Gansu Tech Innovation Center of Animal Cell, Biomedical Research Center, Northwest Minzu University, Lanzhou 730030, China; Key Laboratory of Biotechnology and Bioengineering of State Ethnic Affairs Commission, Biomedical Research Center, Northwest Minzu University, Lanzhou 730030, China. Electronic address: lixiangrong@xbmu.edu.cn.
  • 5 Engineering Research Center of Key Technology and Industrialization of Cell-based Vaccine, Ministry of Education, Biomedical Research Center, Northwest Minzu University, Lanzhou 730030, China; Gansu Tech Innovation Center of Animal Cell, Biomedical Research Center, Northwest Minzu University, Lanzhou 730030, China; Key Laboratory of Biotechnology and Bioengineering of State Ethnic Affairs Commission, Biomedical Research Center, Northwest Minzu University, Lanzhou 730030, China. Electronic address: fengruofei@xbmu.edu.cn.
PMID: 40373618 DOI: 10.1016/j.vetmic.2025.110549
Abstract

EMCV is a significant zoonotic pathogen that causes severe encephalitis and myocarditis, particularly in pigs, posing substantial economic and public health challenges. Nuclear dot protein (NDP) 52 is an important Autophagy adaptor protein known to target microbial pathogens, including viruses into autophagosomes to facilitate the selective Autophagy process. Here, we investigated the interaction between EMCV and NDP52. We found that NDP52 negatively regulates the entry and replication phases of EMCV and interacts with EMCV VP1/VP2 proteins to mediate its autophagic degradation. Moreover, we show that EMCV 2C protein interacts with NDP52 through its N-terminal region to trigger the autophagic degradation of NDP52 via the involvement of the late endosomal molecules, Rab7 and Rab9. Our study reveals a novel mechanism by which EMCV uses its non-structural protein 2C to hijack the Autophagy pathway, evading host Antiviral responses and promoting survival.

Keywords

2C; Autophagy; EMCV; NDP52.

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