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Peer-reviewedCC BYVirulence

Akabane virus reprograms the PKR‑eIF2α‑SGs/PBs axis to fine-tune cap-snatching efficiency.

  • Zhongyin Liu1
  • Dongjie Chen2
  • Jiamin Qin1
  • Jingjing Wang2
  • Di Wang3
  • Wenke Ruan1
  • Shengkui Xu1
  1. 1Beijing Key Laboratory of Traditional Chinese Veterinary Medicine, College of Veterinary Medicine, Beijing University of Agriculture, Beijing, China.
  2. 2Institute of Animal Inspection and Quarantine, Chinese Academy of Quality and Inspection & Testing, Beijing, China.
  3. 3School of Agroforestry and Medicine, The Open University of China, Beijing, China.
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Abstract

Akabane virus (AKAV) initiates transcription in the cytoplasm via the cap-snatching mechanism. Cytoplasmic host mRNAs act as the primary cap donors, whereas the impact of their subcellular localization on the cap-snatching process remains unclear. Herein, we demonstrate that the AKAV-induced disassembly of polysomes, stress granules (SGs), and processing bodies (PBs) collectively facilitates viral cap-snatching. Mechanistically, AKAV infection activates the PKR-eIF2α signaling axis, leading to the disassembly of polysomes and subsequent translational shutoff. Intriguingly, the viral N protein disassembles SGs and PBs by competing for sequestered RNAs within these granules, whereas mutations of its RNA-binding residues abolish this activity. Moreover, PKR-eIF2α inhibition impairs AKAV replication and cap-snatching efficacy. In contrast, inhibition of SGs via G3BP1 knockdown or chemical agents significantly enhances viral replication and cap-snatching efficiency, indicating that polysomes and SGs disassembly favor caps acquisition. Additionally, N protein-mediated PBs disassembly protects mRNA from degradation, and PBs inhibition enhances cap-snatching. Taken together, AKAV has evolved a sophisticated strategy to reprogram mRNA distribution to create an optimal cellular environment for viral cap-snatching.

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Cite

BibTeXRIS
BibTeX
@article{liu2026akabane,
  title = {{Akabane virus reprograms the PKR‑eIF2α‑SGs/PBs axis to fine-tune cap-snatching efficiency.}},
  author = {Zhongyin Liu and Dongjie Chen and Jiamin Qin and Jingjing Wang and Di Wang and Wenke Ruan and Shengkui Xu},
  journal = {Virulence},
  year = {2026},
  month = oct,
  doi = {10.1080/21505594.2026.2748149},
  url = {https://europepmc.org/article/MED/42864310},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Akabane virus reprograms the PKR‑eIF2α‑SGs/PBs axis to fine-tune cap-snatching efficiency.
AU  - Zhongyin Liu
AU  - Dongjie Chen
AU  - Jiamin Qin
AU  - Jingjing Wang
AU  - Di Wang
AU  - Wenke Ruan
AU  - Shengkui Xu
PY  - 2026
DA  - 2026/10/15
JO  - Virulence
DO  - 10.1080/21505594.2026.2748149
UR  - https://europepmc.org/article/MED/42864310
AB  - Akabane virus (AKAV) initiates transcription in the cytoplasm via the cap-snatching mechanism. Cytoplasmic host mRNAs act as the primary cap donors, whereas the impact of their subcellular localization on the cap-snatching process remains unclear. Herein, we demonstrate that the AKAV-induced disassembly of polysomes, stress granules (SGs), and processing bodies (PBs) collectively facilitates viral cap-snatching. Mechanistically, AKAV infection activates the PKR-eIF2α signaling axis, leading to the disassembly of polysomes and subsequent translational shutoff. Intriguingly, the viral N protein disassembles SGs and PBs by competing for sequestered RNAs within these granules, whereas mutations of its RNA-binding residues abolish this activity. Moreover, PKR-eIF2α inhibition impairs AKAV replication and cap-snatching efficacy. In contrast, inhibition of SGs via G3BP1 knockdown or chemical agents significantly enhances viral replication and cap-snatching efficiency, indicating that polysomes and SGs disassembly favor caps acquisition. Additionally, N protein-mediated PBs disassembly protects mRNA from degradation, and PBs inhibition enhances cap-snatching. Taken together, AKAV has evolved a sophisticated strategy to reprogram mRNA distribution to create an optimal cellular environment for viral cap-snatching.
SN  - 2150-5594
SN  - 2150-5608
ER  -