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猪瘟病毒增殖与GBF1和Rab2相关。

CSFV proliferation is associated with GBF1 and Rab2.

作者信息

Liang Wulong, Zheng Minping, Bao Changlei, Zhang Yanming

机构信息

College of Veterinary Medicine, Northwest A and F University, Yangling, Shaanxi 712100, People's Republic of China.

出版信息

J Biosci. 2017 Mar;42(1):43-56. doi: 10.1007/s12038-016-9659-0.

DOI:10.1007/s12038-016-9659-0
PMID:28229964
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7091326/
Abstract

The Golgi apparatus and its resident proteins are utilized and regulated by viruses to facilitate their proliferation. In this study, we investigated Classical swine fever virus (CSFV) proliferation when the function of the Golgi was disturbed. Golgi function was disturbed using chemical inhibitors, namely, brefeldin A (BFA) and golgicide A (GCA), and RNA interfering targets, such as the Golgi-specific BFA-resistance guanine nucleotide exchange factor 1 (GBF1) and Rab2 GTPases. CSFV proliferation was significantly inhibited during RNA replication and viral particle generation after BFA and GCA treatment. CSFV multiplication dynamics were retarded in cells transfected with GBF1 and Rab2 shRNA. Furthermore, CSFV proliferation was promoted by GBF1 and Rab2 overexpression using a lentiviral system. Hence, Golgi function is important for CSFV multiplication, and GBF1 and Rab2 participate in CSFV proliferation. Further studies must investigate Golgi-resident proteins to elucidate the mechanism underlying CSFV replication.

摘要

高尔基体及其驻留蛋白被病毒利用和调控以促进其增殖。在本研究中,我们研究了高尔基体功能受到干扰时经典猪瘟病毒(CSFV)的增殖情况。使用化学抑制剂布雷菲德菌素A(BFA)和高尔基体杀虫剂A(GCA)以及RNA干扰靶点,如高尔基体特异性BFA抗性鸟嘌呤核苷酸交换因子1(GBF1)和Rab2 GTP酶,来干扰高尔基体功能。在BFA和GCA处理后,CSFV在RNA复制和病毒粒子产生过程中的增殖受到显著抑制。在转染了GBF1和Rab2 shRNA的细胞中,CSFV的增殖动力学受到阻碍。此外,使用慢病毒系统过表达GBF1和Rab2可促进CSFV增殖。因此,高尔基体功能对CSFV增殖很重要,GBF1和Rab2参与CSFV增殖。进一步的研究必须研究高尔基体驻留蛋白以阐明CSFV复制的潜在机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90a8/7091326/f11a45a4dda2/12038_2016_9659_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90a8/7091326/7ef2eba2cc58/12038_2016_9659_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90a8/7091326/563baa1c59f4/12038_2016_9659_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90a8/7091326/9ee984122133/12038_2016_9659_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90a8/7091326/55b715506286/12038_2016_9659_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90a8/7091326/006f62544e22/12038_2016_9659_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90a8/7091326/b58e73460160/12038_2016_9659_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90a8/7091326/cfd2691da718/12038_2016_9659_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90a8/7091326/3b14d00bcb3f/12038_2016_9659_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90a8/7091326/f11a45a4dda2/12038_2016_9659_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90a8/7091326/7ef2eba2cc58/12038_2016_9659_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90a8/7091326/563baa1c59f4/12038_2016_9659_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90a8/7091326/9ee984122133/12038_2016_9659_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90a8/7091326/55b715506286/12038_2016_9659_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90a8/7091326/006f62544e22/12038_2016_9659_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90a8/7091326/b58e73460160/12038_2016_9659_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90a8/7091326/cfd2691da718/12038_2016_9659_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90a8/7091326/3b14d00bcb3f/12038_2016_9659_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90a8/7091326/f11a45a4dda2/12038_2016_9659_Fig9_HTML.jpg

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