2. Academic Validation
  3. Comparative RNA-seq analysis of Bovine parainfluenza virus type 3 and its V gene-deleted variant reveals that deletion of the V gene affects autophagy signaling

Comparative RNA-seq analysis of Bovine parainfluenza virus type 3 and its V gene-deleted variant reveals that deletion of the V gene affects autophagy signaling

  • Vet Microbiol. 2026 May:316:110966. doi: 10.1016/j.vetmic.2026.110966.
Yu Han 1,  Ao Wang 1,  Yan Gao 2,  Chongsheng Bai 2,  Minying Ju 2,  Bin Han 2,  Xiaoqi Jing 1,  Chongyang Wang 3,  Shanhui Ren 4
Affiliations

Affiliations

  • 1 College of Advanced Agricultural Sciences, Yulin University, Yulin, Shaanxi 719000, China.
  • 2 Yulin Animal Husbandry and Veterinary Service Center, Yulin, Shaanxi 719000, China.
  • 3 Key Laboratory of Applied Technology on Green-Eco-Healthy Animal Husbandry of Zhejiang Province, Zhejiang Provincial Engineering Research Center for Animal Health Diagnostics & Advanced Technology, Zhejiang International Science and Technology Cooperation Base for Veterinary Medicine and Health Management, China-Australia Joint Laboratory for Animal Health Big Data Analytics, College of Animal Science and Technology & College of Veterinary Medicine of Zhejiang A&F University, 666 Wusu Street, Lin'an District, Hangzhou, Zhejiang 311300, China. Electronic address: [email protected].
  • 4 State Key Laboratory for Animal Disease Control and Prevention, College of Veterinary Medicine, Lanzhou University, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, Gansu 730046, China. Electronic address: [email protected].
PMID: 41793875 DOI: 10.1016/j.vetmic.2026.110966
Abstract

Bovine parainfluenza virus type 3 (BPIV3) is a major respiratory pathogen in cattle, with a substantial economic impact on the global livestock industry. The V protein, a nonstructural accessory protein expressed via RNA editing of the P gene, antagonizes canonical Antiviral signaling. However, its additional role in promoting viral replication remains poorly defined. Here, we demonstrate that the BPIV3 V protein significantly enhances viral replication via a novel autophagy-dependent mechanism. Using a reverse genetics system, we generated a V-gene deletion mutant (rBPIV3-ΔV). Comparative transcriptomic (RNA-seq) analysis of cells infected with wild-type BPIV3 and rBPIV3-ΔV revealed that the V protein specifically modulates host Autophagy signaling. We confirmed key differentially expressed genes using real-time quantitative PCR and identified the V protein as the essential viral factor driving BPIV3-induced Autophagy. Collectively, our transcriptomic data delineate the molecular differences underlying the attenuated replication of rBPIV3-ΔV and establish that the V protein exploits the Autophagy pathway to facilitate viral propagation in vitro. This finding provides a crucial theoretical advance in understanding BPIV3 pathogenesis and reveals potential targets for the development of novel antivirals and vaccines.

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