RNA-dependent protein kinase is required for alpha-1 interferon transgene-induced resistance to genital herpes simplex virus type 2

被引：18

作者：

Carr, DJJ

Tomanek, L

Silverman, RH

Campbell, IL

Williams, BRG

机构：

[1] Univ Oklahoma, Hlth Sci Ctr, Dept Ophthalmol, Oklahoma City, OK 73104 USA

[2] Cleveland Clin Fdn, Lerner Res Inst, Dept Canc Biol, NB40, Cleveland, OH 44195 USA

[3] Cleveland Clin Fdn, Cleveland, OH 44195 USA

[4] Univ Sydney, Sch Mol & Microbial Biosci, Sydney, NSW 2006, Australia

来源：

JOURNAL OF VIROLOGY | 2005年 / 79卷 / 14期

关键词：

D O I：

10.1128/JVI.79.14.9341-9345.2005

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

We investigated the mechanism of resistance to genital herpes simplex virus type 2 (HSV-2) infection in mice transfected with the murine alpha-1 interferon (IFN-alpha 1) transgene. In situ transfection of mice with the IFN-alpha 1 transgene resulted in an elevation in an IFN-responsive gene, RNA-dependent protein kinase (PKR), but not 2 ',5 '-oligoadenylate synthetases (OAS), in vaginal tissue. Coupled with the finding that mice lacking a functional PKR pathway were no longer resistant to genital HSV-2 infection following transfection with the IFN-alpha 1 transgene in comparison to wild-type mice or mice lacking a functional OAS pathway, these results suggest that PKR is the dominant antiviral pathway activated by the IFN-alpha 1 transgene.

引用

页码：9341 / 9345

页数：5

共 32 条

[1]

Akwa Y, 1998, J IMMUNOL, V161, P5016

[2] The murine double-stranded RNA-dependent protein kinase PKR and the murine 2′,5′-oligoadenylate synthetase-dependent RNase L are required for IFN-β-mediated resistance against herpes simplex virus type 1 in primary trigeminal ganglion culture [J].