Role of Us3 gene of herpes simplex virus type 1 for resistance to interferon

The sensitivity of a Us3-deletion mutant virus of herpes simplex virus type 1 (HSV-1) to consensus interferon (IFN) was compared with that of parental wild-type (wt) and the repaired viruses. Although one-step growth of the Us3-deficient virus in the IFN-treated HEp-2 cells was not markedly affected at a high multiplicity of infection (MOI), both the progeny virus yield and cytopathic effect were suppressed in a significantly higher degree in the mutant virus-infected cells than those in wt or the repaired virus-infected cells. This enhanced IFN-sensitivity of the mutant virus was more clearly demonstrated by the infection at a low MOI. In addition, both the size and number of plaques of the Us3-deficient virus in Vero cells were remarkably reduced with increasing concentrations of IFN, compared to those of wt or the repaired virus. These results indicate that the deletion of Us3 gene makes HSV-1 more sensitive to IFN.