Nonmuscle Myosin Heavy Chain IIB Mediates Herpes Simplex Virus 1 Entry

被引：35

作者：

Arii, Jun ^{[1
,2
]}

Hirohata, Yoshitaka ^{[1
,2
]}

Kato, Akihisa ^{[1
,2
]}

Kawaguchi, Yasushi ^{[1
,2
]}

机构：

[1] Univ Tokyo, Inst Med Sci, Dept Microbiol & Immunol, Div Mol Virol, Tokyo, Japan

[2] Univ Tokyo, Inst Med Sci, Int Res Ctr Infect Dis, Dept Infect Dis Control, Tokyo, Japan

来源：

JOURNAL OF VIROLOGY | 2015年 / 89卷 / 03期

基金：

日本学术振兴会;

关键词：

SARCOMA-ASSOCIATED HERPESVIRUS; GREEN FLUORESCENT PROTEIN; TYPE-2; RECEPTOR-ALPHA; CELL-FUSION; HEPARAN-SULFATE; GLYCOPROTEIN-B; EPITHELIAL-CELLS; VIRAL ENTRY; PILR-ALPHA; INTEGRIN ALPHA-V-BETA-3;

D O I：

10.1128/JVI.03079-14

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

Nonmuscle myosin heavy chain IIA (NMHC-IIA) has been reported to function as a herpes simplex virus 1 (HSV-1) entry coreceptor by interacting with viral envelope glycoprotein B (gB). Vertebrates have three genetically distinct isoforms of the NMHCII, designated NMHC-IIA, NMHC-IIB, and NMHC-IIC. COS cells, which are readily infected by HSV-1, do not express NMHC-IIA but do express NMHC-IIB. This observation prompted us to investigate whether NMHC-IIB might associate with HSV-1 gB and be involved in an HSV-1 entry like NMHC-IIA. In these studies, we show that (i) NMHC-IIB coprecipitated with gB in COS-1 cells upon HSV-1 entry; (ii) a specific inhibitor of myosin light chain kinase inhibited cell surface expression of NMHC-IIB in COS-1 cells upon HSV-1 entry as well as HSV-1 infection, as reported with NMHC-IIA; (iii) overexpression of mouse NMHC-IIB in IC21 cells significantly increased their susceptibility to HSV-1 infection; and (iv) knockdown of NMHC-IIB in COS-1 cells inhibited HSV-1 infection as well as cell-cell fusion mediated by HSV-1 envelope glycoproteins. These results supported the hypothesis that, like NMHC-IIA, NMHC-IIB associated with HSV-1 gB and mediated HSV-1 entry.

引用

页码：1879 / 1888

页数：10

共 72 条

[71] A cell surface protein with herpesvirus entry activity (HveB) confers susceptibility to infection by mutants of herpes simplex virus type 1, herpes simplex virus type 2, and pseudorabies virus [J].