Molecular Chaperone BiP Interacts with Borna Disease Virus Glycoprotein at the Cell Surface

被引：51

作者：

Honda, Tomoyuki ^{[1
,2
]}

Horie, Masayuki ^{[1
]}

Daito, Takuji ^{[1
]}

Ikuta, Kazuyoshi ^{[1
]}

Tomonaga, Keizo ^{[1
,3
]}

机构：

[1] Osaka Univ, Res Inst Microbial Dis BIKEN, Dept Virol, Suita, Osaka 5650871, Japan

[2] JSPS, Chiyoda Ku, Tokyo 1028472, Japan

[3] Japan Sci & Technol Agcy, PRESTO, Chiyoda Ku, Tokyo 1020075, Japan

来源：

JOURNAL OF VIROLOGY | 2009年 / 83卷 / 23期

基金：

日本科学技术振兴机构;

关键词：

COXSACKIEVIRUS A9; AXONAL-TRANSPORT; P56; PROTEIN; GRP78; INFECTION; ENTRY; RECEPTOR; NEURONS; DISSEMINATION; EPIDEMIOLOGY;

D O I：

10.1128/JVI.01201-09

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

Borna disease virus (BDV) is characterized by highly neurotropic infection. BDV enters its target cells using virus surface glycoprotein (G), but the cellular molecules mediating this process remain to be elucidated. We demonstrate here that the N-terminal product of G, GP1, interacts with the 78-kDa chaperone protein BiP. BiP was found at the surface of BDV-permissive cells, and anti-BiP antibody reduced BDV infection as well as GP1 binding to the cell surface. We also reveal that BiP localizes at the synapse of neurons. These results indicate that BiP may participate in the cell surface association of BDV.

引用

页码：12622 / 12625

页数：4

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