2. Academic Validation
  3. SEC10 suppresses KLF15-mediated transcriptional activation of JAK1 and promotes BoHV-1 replication

SEC10 suppresses KLF15-mediated transcriptional activation of JAK1 and promotes BoHV-1 replication

  • Vet Microbiol. 2026 May:316:111004. doi: 10.1016/j.vetmic.2026.111004.
Wenqing Ma 1,  Xiao Yu 1,  Yanan Xu 2,  Fachao Sun 1,  Mengrui Zhao 1,  Xinlei Wang 1,  Yanjun Huan 3,  Xin Yin 4,  Hongmei Wang 5,  Hongbin He 6
Affiliations

Affiliations

  • 1 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; Department of Preventive Veterinary Medicine, College of Veterinary Medicine, Shandong Agricultural University, Taian 271018, PR China.
  • 3 College of Veterinary Medicine, Qingdao Agricultural University, Qingdao 266109, PR China.
  • 4 Division of Livestock Infectious Diseases, State Key Laboratory for Animal Disease Control and Prevention, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin 150069, PR China.
  • 5 Ruminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan 250358, PR China. Electronic address: [email protected].
  • 6 Ruminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan 250358, PR China. Electronic address: [email protected].
PMID: 41903488 DOI: 10.1016/j.vetmic.2026.111004
Abstract

SEC10 (EXOC5), a central subunit of the exocyst complex, plays a critical role in vesicle trafficking. However, its function in bovine herpesvirus 1 (BoHV-1) triggered-antiviral innate immunity and viral replication remains unclear. In this study, we identify SEC10 as a key negative regulator of Antiviral immune responses. SEC10 suppresses the transcriptional expression of JAK1, thereby significantly impairing activation of the JAK-STAT signaling pathway, dampening type I interferon (IFN-I)-mediated Antiviral immunity, and promoting BoHV-1 replication. Mechanistically, SEC10 downregulates the expression of the transcription factor KLF15 and subsequently modulates JAK1 transcription in a KLF15-dependent manner, establishing a "SEC10-KLF15-JAK1" regulatory axis. Collectively, our findings not only reveal SEC10 as a novel immunomodulatory factor but also uncover a previously unrecognized KLF15-dependent transcriptional mechanism that fine-tunes innate immune responses. This work provides new insights into the complex regulatory network of the JAK-STAT signaling pathway and identifies a potential therapeutic target for combating BoHV-1 Infection.

Keywords

Antiviral innate immunity; BoHV-1; JAK1; KLF15; SEC10.

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