Open AccessRNA-Dependent Protein Kinase Is Required for Alpha-1 Interferon Transgene-Induced Resistance to Genital Herpes Simplex Virus Type 2
Author(s) -
Daniel J. J. Carr,
Lisa Tomanek,
Robert H. Silverman,
Iain L. Campbell,
Bryan R.G. Williams
Publication year - 2005
Publication title -
journal of virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.617
H-Index - 292
eISSN - 1070-6321
pISSN - 0022-538X
DOI - 10.1128/jvi.79.14.9341-9345.2005
Subject(s) - biology , virology , herpes simplex virus , transgene , interferon type i , antiviral protein , protein kinase r , interferon , protein kinase a , alpha interferon , virus , alpha (finance) , rna , eif 2 kinase , kinase , microbiology and biotechnology , gene , mitogen activated protein kinase kinase , genetics , cyclin dependent kinase 2 , medicine , construct validity , nursing , patient satisfaction
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-alpha1) transgene. In situ transfection of mice with the IFN-alpha1 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-alpha1 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-alpha1 transgene.