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. 2002 May;76(10):5251–5259. doi: 10.1128/JVI.76.10.5251-5259.2002

FIG. 2.

FIG. 2.

Impact of RNase L and PKR deficiencies on viral growth and pathogenesis. (A) One-step growth of VV and VVΔE3L (Copenhagen strain) in wild-type and RNase L−/− PKR−/− cells. Cells were infected at an MOI of 6. At different times postinfection, viruses were harvested and virus yields were determined by plaque titration on BHK21 cells. (B) VV but not VVΔE3L is lethal for mice regardless of the presence or absence of RNase L and PKR. Seven-week-old wild-type, RNase L−/−, PKR−/−, and RNase L−/− PKR−/− mice were injected i.n. with 106 PFU of wild-type VV or 5 × 106 PFU of VVΔE3L (WR strain). Survival was monitored daily, and the mouse survival was plotted.