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Differential effect of murine alpha/beta interferon transgenes on antagonization of herpes simplex virus type 1 replication

Harle, P., Cull, V., Agbaga, M-P, Silverman, R., Williams, B.R.G., James, C. and Carr, D.J.J. (2002) Differential effect of murine alpha/beta interferon transgenes on antagonization of herpes simplex virus type 1 replication. Journal of Virology, 76 (13). pp. 6558-6567.

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Alpha/beta interferons (IFN-α/β) are potent, endogenous antiviral cytokines that suppress the replication of RNA and DNA viruses, including herpes simplex virus type 1 (HSV-1). The present study compared the efficacies of IFN-α/β transgenes, including IFN-α1, -α4, -α5, -α6, -α9, and -β, against HSV-1 infection. L929 cells transfected with the IFN-α/β transgenes produced similar levels of IFN, as measured by bioassay and enzyme-linked immunosorbent assay. In addition, transfected cells were less susceptible to HSV-1 infection than were cells transfected with a plasmid vector control. The murine IFN-β plasmid construct exhibited the greatest reduction, while the murine IFN-α5 transgene showed a modest inhibitory effect in viral titers recovered from the supernatants of transfected, infected L929 cultures. Consistent with this observation, the IFN-β transgene antagonized viral transcript levels, including infected cell protein 27, thymidine kinase, and glycoprotein B, to a greater extent than did the IFN-α transgenes at 6 to 10 h postinfection as determined by real-time PCR. Cells transfected with the IFN-α4, IFN-α9, or IFN-β transgenes showed the greatest reduction in viral protein expression relative to the other transfected cells, which was associated with increased STAT1 expression. The absence of the IFN-responsive protein kinase R (PKR) gene completely abrogated the antiviral induction by all IFN-α/β against HSV-1. In the absence of RNase L, viral yields were increased 10-fold, but the antiviral effect of IFN was either unaffected or enhanced. These results suggest that the predominant IFNmediated, antiviral pathway during HSV-1 infection taken by IFN-α/β in L929 cells utilizes PKR.

Item Type: Journal Article
Murdoch Affiliation(s): School of Veterinary and Biomedical Sciences
Publisher: American Society for Microbiology
Copyright: © 2002, American Society for Microbiology
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