THE BG II-N FRAGMENT OF HERPES-SIMPLEX VIRUS TYPE-2 CONTAINS A REGIONRESPONSIBLE FOR RESISTANCE TO ANTIVIRAL EFFECTS OF INTERFERON/

Double infection with two interferon (IFN)-sensitive strains of herpes simplex virus (HSV), HSV-1 (17 syn) and HSV-2(UW268), showed reduced inhibition of virus growth by IFN. Intertypic recombinants with IFN re sistance were obtained from the doubly infected cultures, These result s indicate that HSV IFN resistance is controlled by at least two genet ic regions, Restriction endonuclease analysis demonstrated that the re combinants were similar to HSV-2 in their genomic structure but the Ba mHI-A, BglII-I and BglII-N fragments of HSV-2 were commonly lost in th e recombinants, suggesting that any of these fragments could be associ ated with HSV-2 IFN resistance, We cloned these fragments and BamHI-E, which overlaps BglII-N, from an IFN-resistant HSV-2 strain, HSV-2(G), and examined each fragment for its ability to rescue IFN resistance o f HSV-2(UW268) by co-transfecting with the HSV-2(UW268) genome. Of the HSV-2(G) fragments, only BglII-N increased plating efficiency of prog eny viruses in IFN-treated cells. An IFN-resistant HSV-2 clone was obt ained from the BglII-N of HSV-2(G) and HSV-2(UW268) genome co-transfec ted culture, and a part of BglII-N of HSV-2(UW268) was replaced with t hat of HSV-2(G) in the HSV-2 clone. Thus, it was concluded that one of the HSV regions encoding IFN resistance is located on the BglII-N fra gment of HSV-2.