The defect in Stat 1 rendered rag2-/- stat1-/- mice incapable of limiting HSV-1 spread, and these mice succumbed to the viral infection just 7.8 ± 1 days p.i. In contrast, the weakly virulent KOS-GFP strain [50] caused a slowly progressing infection in rag2-/- mice that was not lethal until 25 ± 2 days p.i. Thus, Stat 1 plays an integral role in innate resistance to HSV-1 infection. This evidence concerns the gene STAT1 and viral infectious disease.