Nervous necrosis virus B2 non-structural protein shut off host translation via sequestration of polyadenylate-binding protein
Journal
Biochemical and Biophysical Research Communications
Journal Volume
827
Start Page
154020
ISSN
0006-291X
Date Issued
2026-08-20
Author(s)
Bajpai, Vertika
Lin, I-Wen
Chiang, Ming-Hsien
Li, Chen-Hung
Chen, Chien-Wen
Chang, Chia-Ching
Cheng, Chao-An
Chen, Shih-Chieh
Chang, Chi-Yao
Abstract
Nervous necrosis virus (NNV) is the causative agent of viral nervous necrosis disease in piscine larvae worldwide. As a positive-sense RNA virus, NNV performs its replication, transcription, translation and assembly in the cytoplasm of host cell. However, the ectopic expression of viral B2 non-structural protein was observed to translocate into nucleus of grouper brain cells. In this study, we found that the nuclear translocation of B2 was accompanied by host translation shutoff which was examined by the surface sensing of translation (SUnSET) puromycin labelling experiment. Furthermore, the ectopically expressed B2 protein was also observed to co-localize with polyadenylate-binding protein (PABP) in cytoplasm and nucleus of transfected cell. The far-Western blotting further confirmed the interaction between B2 and PABP. Finally, the decrease in B2 protein levels at the late stage of infection appears to result from lysosome-mediated degradation facilitated by its interaction with Mx proteins. These results reveal that NNV B2 non-structural protein contributes to host translation shutoff after infection.
Subjects
B2
Lysosome
Mx
Nervous necrosis virus
Polyadenylate-binding protein
Translation shutoff
Publisher
Elsevier BV
Type
journal article