BVDV non-structural protein 4B promoted autophagy by regulating p62/LC3-II molecule

Beiyan Wang; Kaiyue Liu; Shuyu Wei; Min Wang; Jiacheng Zhou; Shuangshuang Wu; Yazun Dong; Yixuan Ma; Hongyan Liu; Liquan Yu; Jinzhu Ma; Baifen Song

doi:10.1016/j.vetimm.2025.110973

BVDV non-structural protein 4B promoted autophagy by regulating p62/LC3-II molecule

Vet Immunol Immunopathol. 2025 Jun 26:286:110973. doi: 10.1016/j.vetimm.2025.110973. Online ahead of print.

Authors

Affiliations

¹ College of Life Science and Biotechnology, Heilongjiang Bayi Agricultural University, Daqing, China.
² College of Life Science and Biotechnology, Heilongjiang Bayi Agricultural University, Daqing, China. Electronic address: majinzhu1976@163.com.
³ Key Laboratory of Animal Epidemiology and Zoonosis, College of Veterinary Medicine, China Agricultural University, Beijing, China. Electronic address: songbaifen0819@163.com.

PMID: 40580697
DOI: 10.1016/j.vetimm.2025.110973

Abstract

Bovine viral diarrhea virus (BVDV) causes bovine viral diarrhea-mucosal disease that is characterized by diarrhea, fever, leukopenia, and propagation disorders in host animals. Autophagy acts an important regulatory role during virial infection. However, the molecular mechanisms that BVDV induces autophagy remain poorly defined. Here, we report that BVDV non-structural protein 4B (NS4B) promotes autophagy in MDBK cells and HEK-293T cells by reducing the level of p62 protein and increasing the production of LC3-II protein, and NS4B proteins were able to improve autophagy in MDBK cells by inhibiting the phosphorylation of mTOR protein. In addition, NS4B (90-260aa) acts a main role in promoting autophagy. The results reveal a new mechanism of BVDV to induce autophagy in host cells and also provide a new theoretical basis for the interaction between BVDV and host cells, and an important target for the prevention and control of BVDV.

Keywords: Autophagy; Bovine viral diarrhea Virus; LC3-I; LC3-II; MTOR; P62.