2. Academic Validation
  3. BoHV-1 UL3 inhibits RLR signaling response by degrading MAVS

BoHV-1 UL3 inhibits RLR signaling response by degrading MAVS

  • Vet Microbiol. 2025 Nov 10:312:110791. doi: 10.1016/j.vetmic.2025.110791.
Yanan Xu 1,  Wenqing Ma 2,  Hongmei Wang 3,  Hongbin He 4
Affiliations

Affiliations

  • 1 Department of Preventive Veterinary Medicine, College of Veterinary Medicine, Shandong Agricultural University, Taian 271018, PR China; Ruminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan 250358, PR China.
  • 2 Ruminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan 250358, PR China.
  • 3 Ruminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan 250358, PR China. Electronic address: [email protected].
  • 4 Ruminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan 250358, PR China. Electronic address: [email protected].
PMID: 41223816 DOI: 10.1016/j.vetmic.2025.110791
Abstract

Bovine herpesvirus 1 (BoHV-1) Infection can lead to host immunosuppression, and its tegument proteins play a critical role in suppressing Antiviral immune responses. However, the mechanisms by which BoHV-1 tegument proteins modulate the RLR signaling pathway and influence the replication of bovine RNA viruses remain poorly understood. Here, we demonstrated that BoHV-1 tegument protein UL3 significantly suppresses BPIV3 infection-trigged RLR signaling response and promotes virus replication. Through in-depth mechanistic investigations, we found that UL3 upregulates the expression of Smurf2, thereby enhancing the polyubiquitination of MAVS. This modification targets MAVS for proteasomal degradation and subsequent degradation. Notably, the knockdown of Smurf2 rescues MAVS from degradation. Collectively, our findings unveil a previously uncharacterized mechanism by which BoHV-1 UL3 enables BPIV3 to evade the host innate immune surveillance system.

Keywords

Antiviral innate immunity; BPIV3; BoHV-1 UL3; MAVS; Smurf2.

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