1. Academic Validation
  2. Mitochondria-mediated ferroptosis contributes to the inflammatory responses of bovine viral diarrhea virus (BVDV) in vitro

Mitochondria-mediated ferroptosis contributes to the inflammatory responses of bovine viral diarrhea virus (BVDV) in vitro

  • J Virol. 2024 Jan 16:e0188023. doi: 10.1128/jvi.01880-23.
Zhijun Li # 1 2 Bao Zhao # 1 3 Ying Zhang 1 2 Wenqi Fan 1 2 Qinghong Xue 4 Xiwen Chen 5 Jingyu Wang 1 2 Xuefeng Qi 1 2
Affiliations

Affiliations

  • 1 College of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, China.
  • 2 Key Laboratory of Ruminant Disease Prevention and Control (West), Ministry of Agriculture and Rural Affairs, Xi'an, China.
  • 3 Shaanxi Animal Disease Control Center, Xi'an, China.
  • 4 China Institute of Veterinary Drug Control, Beijing, China.
  • 5 Animal Disease Prevention and Control, Healthy Breeding Engineering Technology Research Center, Mianyang Normal University, Mianyang, Sichuan, China.
  • # Contributed equally.
Abstract

Bovine viral diarrhea virus (BVDV) threatens a wide range of domestic and wild cattle population worldwide. BVDV causes great economic loss in cattle industry through its immunosuppression and persistent Infection. Despite extensive research, the mechanism underlying the pathogenesis of BVDV remains elusive. Our data provide the first direct evidence that mitochondria-mediated Ferroptosis and Mitophagy are involved in inflammatory responses in both biotypes of BVDV-infected cells. Importantly, we demonstrate that the different degrees of injury of mitochondria and inflammatory responses may attribute to different Mitophagy pathways induced by biotypes of BVDV. Overall, our findings uncover the interaction between BVDV Infection and mitochondria-mediated Ferroptosis, which shed novel LIGHT on the physiological impacts of Ferroptosis on the pathogenesis of BVDV Infection, and provide a promising therapeutic strategy to treat this important infectious disease with a worldwide distribution.

Keywords

BVDV; ferroptosis; inflammatory responses; mitochondria damage; mitophagy.

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