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Cholesterol Biosynthesis Modulates CSFV Replication

Classical swine fever (CSF) caused by the classical swine fever virus (CSFV) has resulted in severe losses to the pig industry worldwide. It has been proposed that lipid synthesis is essential for viral replication, and lipids are involved in viral protein maturation and envelope production. However...

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Autores principales: Zou, Xiaodong, Lin, Feng, Yang, Yang, Chen, Jiahuan, Zhang, Huanyu, Li, Linquan, Ouyang, Hongsheng, Pang, Daxin, Tang, Xiaochun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9316236/
https://www.ncbi.nlm.nih.gov/pubmed/35891429
http://dx.doi.org/10.3390/v14071450
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author Zou, Xiaodong
Lin, Feng
Yang, Yang
Chen, Jiahuan
Zhang, Huanyu
Li, Linquan
Ouyang, Hongsheng
Pang, Daxin
Tang, Xiaochun
author_facet Zou, Xiaodong
Lin, Feng
Yang, Yang
Chen, Jiahuan
Zhang, Huanyu
Li, Linquan
Ouyang, Hongsheng
Pang, Daxin
Tang, Xiaochun
author_sort Zou, Xiaodong
collection PubMed
description Classical swine fever (CSF) caused by the classical swine fever virus (CSFV) has resulted in severe losses to the pig industry worldwide. It has been proposed that lipid synthesis is essential for viral replication, and lipids are involved in viral protein maturation and envelope production. However, the specific crosstalk between CSFV and host cell lipid metabolism is still unknown. In this study, we found that CSFV infection increased intracellular cholesterol levels in PK-15 cells. Further analysis demonstrated that CSFV infection upregulated PCSK9 expression to block the uptake of exogenous cholesterol by LDLR and enhanced the cholesterol biosynthesis pathway, which disrupted the type I IFN response in PK-15 cells. Our findings provide new insight into the mechanisms underpinning the pathogenesis of CSFV and hint at methods for controlling the disease.
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spelling pubmed-93162362022-07-27 Cholesterol Biosynthesis Modulates CSFV Replication Zou, Xiaodong Lin, Feng Yang, Yang Chen, Jiahuan Zhang, Huanyu Li, Linquan Ouyang, Hongsheng Pang, Daxin Tang, Xiaochun Viruses Article Classical swine fever (CSF) caused by the classical swine fever virus (CSFV) has resulted in severe losses to the pig industry worldwide. It has been proposed that lipid synthesis is essential for viral replication, and lipids are involved in viral protein maturation and envelope production. However, the specific crosstalk between CSFV and host cell lipid metabolism is still unknown. In this study, we found that CSFV infection increased intracellular cholesterol levels in PK-15 cells. Further analysis demonstrated that CSFV infection upregulated PCSK9 expression to block the uptake of exogenous cholesterol by LDLR and enhanced the cholesterol biosynthesis pathway, which disrupted the type I IFN response in PK-15 cells. Our findings provide new insight into the mechanisms underpinning the pathogenesis of CSFV and hint at methods for controlling the disease. MDPI 2022-06-30 /pmc/articles/PMC9316236/ /pubmed/35891429 http://dx.doi.org/10.3390/v14071450 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Zou, Xiaodong
Lin, Feng
Yang, Yang
Chen, Jiahuan
Zhang, Huanyu
Li, Linquan
Ouyang, Hongsheng
Pang, Daxin
Tang, Xiaochun
Cholesterol Biosynthesis Modulates CSFV Replication
title Cholesterol Biosynthesis Modulates CSFV Replication
title_full Cholesterol Biosynthesis Modulates CSFV Replication
title_fullStr Cholesterol Biosynthesis Modulates CSFV Replication
title_full_unstemmed Cholesterol Biosynthesis Modulates CSFV Replication
title_short Cholesterol Biosynthesis Modulates CSFV Replication
title_sort cholesterol biosynthesis modulates csfv replication
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9316236/
https://www.ncbi.nlm.nih.gov/pubmed/35891429
http://dx.doi.org/10.3390/v14071450
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