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. Author manuscript; available in PMC: 2014 Jun 17.
Published in final edited form as: J Immunol. 2004 May 1;172(9):5638–5647. doi: 10.4049/jimmunol.172.9.5638

Figure 7. The absence of PKR reduces but does not eliminate the anti-viral action of the Ad:IFN-β vector against ocular HSV-1 infection while the absence of a functional OAS pathway transiently reduces the anti-viral efficacy of the Ad:IFN-β vector in the cornea.

Figure 7

Wild type (WT) and mice deficient in RNase L (RL−/−) or PKR (PKR−/−) (n=4 per group/experiment) were transduced with Ad:IFN-β (dotted column) or Ad:Null vectors (black column) (1 × 106 transducing units/eye). Two days later, the mice were infected with HSV-1 (600 pfu/eye). Mice were euthanized 3 or 6 days post infection, and the cornea (A, C) and the TG (B, D) were removed. The tissue was homogenized and the clarified homogenate (10,000 × g, 1 min) was quantified for infectious virus by plaque assay. Results are a summary of three independent experiments. Bars represent the log of the mean +/− SEM. *p<.05 comparing the Ad:IFN-β to the Ad:Null treated mice.