2. Academic Validation
  3. Akabane virus infection induces PABP1 nuclear retention and inhibits IFN-β production

Akabane virus infection induces PABP1 nuclear retention and inhibits IFN-β production

  • Virology. 2026 Jun:619:110878. doi: 10.1016/j.virol.2026.110878.
Zhongyin Liu 1,  Jiamin Qin 1,  Yao Zhao 1,  Tianai Zhang 1,  Shucheng Zong 2,  Xiaoyan Wang 3,  Wenke Ruan 1,  Dongjie Chen 4,  Shengkui Xu 5
Affiliations

Affiliations

  • 1 Beijing Key Laboratory of Traditional Chinese Veterinary Medicine, College of Animal Science and Technology, Beijing University of Agriculture, Beijing, 102206, People's Republic of China.
  • 2 Key Laboratory of Veterinary Biological Products and Chemical Drugs, Ministry of Agriculture and Rural Affairs, Engineering and Technology Research Center for Beijing Veterinary Peptide Vaccine Design and Preparation, Zhongmu Institutes of China Animal Husbandry Industry Co. Ltd, Beijing, 100095, People's Republic of China.
  • 3 College of Veterinary Medicine, China Agricultural University, Beijing, 100193, People's Republic of China.
  • 4 Institute of Animal Inspection and Quarantine, Chinese Academy of Quality and Inspection & Testing, Beijing, 100176, People's Republic of China. Electronic address: [email protected].
  • 5 Beijing Key Laboratory of Traditional Chinese Veterinary Medicine, College of Animal Science and Technology, Beijing University of Agriculture, Beijing, 102206, People's Republic of China. Electronic address: [email protected].
PMID: 41880901 DOI: 10.1016/j.virol.2026.110878
Abstract

Akabane virus (AKAV), a member of the Orthobunyavirus genus in Peribunyaviridae family, primarily infects ruminants such as cattle and sheep. AKAV mRNAs are capped but not polyadenylated, a feature that distinguishes them from host mRNAs. Poly(A)-binding protein 1 (PABP1) regulates eukaryotic mRNA translation by binding to host mRNA poly(A) tail, which is often hijacked by viruses. Here, its role during AKAV Infection was investigated. Our study demonstrated that AKAV Infection induced PABP1 nuclear retention at the late stage of Infection, which in turn triggered the shutdown of host cell translation. Moreover, we found that ectopic expression of the AKAV N protein induced PABP1 nuclear sequestration, while AKAV N protein partially colocalized with PABP1 at the early stage of Infection. However, disruption of the N protein's RNA-binding domain (RBD) via amino acid mutation severely impaired its ability to retain PABP1 in the nucleus, suggesting that the AKAV N protein may compete with PABP1 for mRNA binding, thereby promoting the translocation of unbound PABP1 into the nucleus. Additionally, AKAV Infection upregulated IFN-β transcription yet attenuated poly(I: C)-triggered IFN-β translation, and N protein also exhibited such an effect. Together, the AKAV N protein induces nuclear relocation of PABP1 and inhibits IFN-β expression to promote viral replication.

Keywords

AKAV; IFN-β; N protein; Nuclear translocation; PABP1.

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