Classical swine fever virus-Shimen infection upregulates SH3GLB1 expression in porcine alveolar macrophages

Although SH3GLB1 is well known as an autophagy-related protein, its response mechanism to virus infection has yet to be determined. Through digital gene expression (DGE) profile analysis, we identified that SH3GLB1 may be a key gene responding to classical swine fever virus (CSFV) infection in porci...

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Main Authors: Aoxue Hu, Xuepeng Li, Jun He, Xiaocheng Gong, Zhongxing Wu, Pengbo Ning
Format: Article
Language:English
Published: Taylor & Francis Group 2019-01-01
Series:Biotechnology & Biotechnological Equipment
Subjects:
Online Access:http://dx.doi.org/10.1080/13102818.2018.1552839
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spelling doaj-9dfc68b0082842248a8c115de4de1f622020-11-25T00:12:56ZengTaylor & Francis GroupBiotechnology & Biotechnological Equipment1310-28181314-35302019-01-01331939710.1080/13102818.2018.15528391552839Classical swine fever virus-Shimen infection upregulates SH3GLB1 expression in porcine alveolar macrophagesAoxue Hu0Xuepeng Li1Jun He2Xiaocheng Gong3Zhongxing Wu4Pengbo Ning5Xidian UniversityXidian UniversityXidian UniversityXidian UniversityXidian UniversityXidian UniversityAlthough SH3GLB1 is well known as an autophagy-related protein, its response mechanism to virus infection has yet to be determined. Through digital gene expression (DGE) profile analysis, we identified that SH3GLB1 may be a key gene responding to classical swine fever virus (CSFV) infection in porcine alveolar macrophages (PAMs). The present study found that the mRNA expression and the SH3GLB1 protein level in CSFV Shimen infected PAMs were significantly higher than those of mock-infected PAMs. Furthermore, confocal microscopy analysis suggested that SH3GLB1 was temporally co-localised with CSFV E2. These findings contributed in developing our understanding of the mechanism of CSFV infection.http://dx.doi.org/10.1080/13102818.2018.1552839csfv shimensh3glb1macrophages
collection DOAJ
language English
format Article
sources DOAJ
author Aoxue Hu
Xuepeng Li
Jun He
Xiaocheng Gong
Zhongxing Wu
Pengbo Ning
spellingShingle Aoxue Hu
Xuepeng Li
Jun He
Xiaocheng Gong
Zhongxing Wu
Pengbo Ning
Classical swine fever virus-Shimen infection upregulates SH3GLB1 expression in porcine alveolar macrophages
Biotechnology & Biotechnological Equipment
csfv shimen
sh3glb1
macrophages
author_facet Aoxue Hu
Xuepeng Li
Jun He
Xiaocheng Gong
Zhongxing Wu
Pengbo Ning
author_sort Aoxue Hu
title Classical swine fever virus-Shimen infection upregulates SH3GLB1 expression in porcine alveolar macrophages
title_short Classical swine fever virus-Shimen infection upregulates SH3GLB1 expression in porcine alveolar macrophages
title_full Classical swine fever virus-Shimen infection upregulates SH3GLB1 expression in porcine alveolar macrophages
title_fullStr Classical swine fever virus-Shimen infection upregulates SH3GLB1 expression in porcine alveolar macrophages
title_full_unstemmed Classical swine fever virus-Shimen infection upregulates SH3GLB1 expression in porcine alveolar macrophages
title_sort classical swine fever virus-shimen infection upregulates sh3glb1 expression in porcine alveolar macrophages
publisher Taylor & Francis Group
series Biotechnology & Biotechnological Equipment
issn 1310-2818
1314-3530
publishDate 2019-01-01
description Although SH3GLB1 is well known as an autophagy-related protein, its response mechanism to virus infection has yet to be determined. Through digital gene expression (DGE) profile analysis, we identified that SH3GLB1 may be a key gene responding to classical swine fever virus (CSFV) infection in porcine alveolar macrophages (PAMs). The present study found that the mRNA expression and the SH3GLB1 protein level in CSFV Shimen infected PAMs were significantly higher than those of mock-infected PAMs. Furthermore, confocal microscopy analysis suggested that SH3GLB1 was temporally co-localised with CSFV E2. These findings contributed in developing our understanding of the mechanism of CSFV infection.
topic csfv shimen
sh3glb1
macrophages
url http://dx.doi.org/10.1080/13102818.2018.1552839
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