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Journal of Virology, July 2005, p. 9341-9345, Vol. 79, No. 14
0022-538X/05/$08.00+0 doi:10.1128/JVI.79.14.9341-9345.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Department of Ophthalmology, Microbiology, and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104,1 Department of Cancer Biology/NB40, Lerner Research Institute, The Cleveland Clinic Foundation, Cleveland, Ohio 44195,2 School of Molecular and Microbial Biosciences, The University of Sydney, NSW 2006, Australia3
Received 22 February 2005/ Accepted 28 March 2005
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-
1) transgene. In situ transfection of mice with the IFN-
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-
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-
1 transgene.
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