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Seneca Valley Virus 3C(pro) Cleaves Heterogeneous Nuclear Ribonucleoprotein K to Facilitate Viral Replication

Seneca Valley virus (SVV) has emerged as an important pathogen that is associated with idiopathic vesicular infection in pigs, causing a potential threat to the global swine industry. The heterogeneous nuclear ribonucleoprotein K (hnRNP K) that shuttles between the nucleus and cytoplasm plays an imp...

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Autores principales: Song, Jiangwei, Quan, Rong, Wang, Dan, Liu, Jue
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9298500/
https://www.ncbi.nlm.nih.gov/pubmed/35875542
http://dx.doi.org/10.3389/fmicb.2022.945443
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author Song, Jiangwei
Quan, Rong
Wang, Dan
Liu, Jue
author_facet Song, Jiangwei
Quan, Rong
Wang, Dan
Liu, Jue
author_sort Song, Jiangwei
collection PubMed
description Seneca Valley virus (SVV) has emerged as an important pathogen that is associated with idiopathic vesicular infection in pigs, causing a potential threat to the global swine industry. The heterogeneous nuclear ribonucleoprotein K (hnRNP K) that shuttles between the nucleus and cytoplasm plays an important role in viral infection. In this study, we observed that infection with SVV induced cleavage, degradation, and cytoplasmic redistribution of hnRNP K in cultured cells, which was dependent on the activity of viral 3C(pro) protease. Also, the 3C(pro) induced degradation of hnRNP K via the caspase pathway. Further studies demonstrated that SVV 3C(pro) cleaved hnRNP K at residue Q364, and the expression of the cleavage fragment hnRNP K (aa.365–464) facilitates viral replication, which is similar to full-length hnRNP K, whereas hnRNP K (aa.1–364) inhibits viral replication. Additionally, hnRNP K interacts with the viral 5′ untranslated region (UTR), and small interfering RNA (siRNA)-mediated knockdown of hnRNP K results in significant inhibition of SVV replication. Overall, our results demonstrated that the hnRNP K positively regulates SVV replication in a protease activity-dependent fashion in which the cleaved C-terminal contributes crucially to the upregulation of SVV replication. This finding of the role of hnRNP K in promoting SVV propagation provides a novel antiviral strategy to utilize hnRNP K as a potential target for therapy.
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spelling pubmed-92985002022-07-21 Seneca Valley Virus 3C(pro) Cleaves Heterogeneous Nuclear Ribonucleoprotein K to Facilitate Viral Replication Song, Jiangwei Quan, Rong Wang, Dan Liu, Jue Front Microbiol Microbiology Seneca Valley virus (SVV) has emerged as an important pathogen that is associated with idiopathic vesicular infection in pigs, causing a potential threat to the global swine industry. The heterogeneous nuclear ribonucleoprotein K (hnRNP K) that shuttles between the nucleus and cytoplasm plays an important role in viral infection. In this study, we observed that infection with SVV induced cleavage, degradation, and cytoplasmic redistribution of hnRNP K in cultured cells, which was dependent on the activity of viral 3C(pro) protease. Also, the 3C(pro) induced degradation of hnRNP K via the caspase pathway. Further studies demonstrated that SVV 3C(pro) cleaved hnRNP K at residue Q364, and the expression of the cleavage fragment hnRNP K (aa.365–464) facilitates viral replication, which is similar to full-length hnRNP K, whereas hnRNP K (aa.1–364) inhibits viral replication. Additionally, hnRNP K interacts with the viral 5′ untranslated region (UTR), and small interfering RNA (siRNA)-mediated knockdown of hnRNP K results in significant inhibition of SVV replication. Overall, our results demonstrated that the hnRNP K positively regulates SVV replication in a protease activity-dependent fashion in which the cleaved C-terminal contributes crucially to the upregulation of SVV replication. This finding of the role of hnRNP K in promoting SVV propagation provides a novel antiviral strategy to utilize hnRNP K as a potential target for therapy. Frontiers Media S.A. 2022-07-06 /pmc/articles/PMC9298500/ /pubmed/35875542 http://dx.doi.org/10.3389/fmicb.2022.945443 Text en Copyright © 2022 Song, Quan, Wang and Liu. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Microbiology
Song, Jiangwei
Quan, Rong
Wang, Dan
Liu, Jue
Seneca Valley Virus 3C(pro) Cleaves Heterogeneous Nuclear Ribonucleoprotein K to Facilitate Viral Replication
title Seneca Valley Virus 3C(pro) Cleaves Heterogeneous Nuclear Ribonucleoprotein K to Facilitate Viral Replication
title_full Seneca Valley Virus 3C(pro) Cleaves Heterogeneous Nuclear Ribonucleoprotein K to Facilitate Viral Replication
title_fullStr Seneca Valley Virus 3C(pro) Cleaves Heterogeneous Nuclear Ribonucleoprotein K to Facilitate Viral Replication
title_full_unstemmed Seneca Valley Virus 3C(pro) Cleaves Heterogeneous Nuclear Ribonucleoprotein K to Facilitate Viral Replication
title_short Seneca Valley Virus 3C(pro) Cleaves Heterogeneous Nuclear Ribonucleoprotein K to Facilitate Viral Replication
title_sort seneca valley virus 3c(pro) cleaves heterogeneous nuclear ribonucleoprotein k to facilitate viral replication
topic Microbiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9298500/
https://www.ncbi.nlm.nih.gov/pubmed/35875542
http://dx.doi.org/10.3389/fmicb.2022.945443
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