ARF1 and GBF1 Generate a PI4P-Enriched Environment Supportive of Hepatitis C Virus Replication

被引：51

作者：

Zhang, Leiliang ^{[1
,2
,3
]}

Hong, Zhi ^{[1
,2
]}

Lin, Wenyu ^{[3
]}

Shao, Run-Xuan ^{[3
]}

Goto, Kaku ^{[3
]}

Hsu, Victor W. ^{[4
,5
]}

Chung, Raymond T. ^{[3
]}

机构：

[1] Chinese Acad Med Sci, Inst Pathogen Biol, Beijing 100730, Peoples R China

[2] Peking Union Med Coll, Beijing 100021, Peoples R China

[3] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Gastrointestinal Unit,Dept Med, Boston, MA USA

[4] Harvard Univ, Brigham & Womens Hosp, Div Rheumatol Immunol & Allergy, Sch Med, Boston, MA 02115 USA

[5] Harvard Univ, Sch Med, Dept Med, Boston, MA USA

来源：

PLOS ONE | 2012年 / 7卷 / 02期

基金：

美国国家卫生研究院;

关键词：

GENOTYPE; 1; INFECTION; 4-KINASE III ALPHA; TELAPREVIR; PEGINTERFERON; REGULATORS; RIBAVIRIN; LIPIDS; TRAFFICKING; RECRUITMENT; PHOSPHATASE;

D O I：

10.1371/journal.pone.0032135

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Cellular levels of phosphatidylinositol 4-phosphate (PI4P) have been shown to be upregulated during RNA replication of several viruses, including the HCV replicon model. However, whether PI4P is required in an infectious HCV model remains unknown. Moreover, it is not established whether the host transport machinery is sequestered by the generation of PI4P during HCV infection. Here we found that PI4P was enriched in HCV replication complexes when Huh7.5.1 cells were infected with JFH1. HCV replication was inhibited upon overexpression of the PI4P phosphatase Sac1. The PI4P kinase PI4KIII beta was also found to be required for HCV replication. Moreover, the vesicular transport proteins ARF1 and GBF1 colocalized with PI4KIII beta and were both required for HCV replication. During authentic HCV infection, PI4P plays an integral role in virus replication.

引用

页数：9

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