M. Narita et al., THE BG II-N FRAGMENT OF HERPES-SIMPLEX VIRUS TYPE-2 CONTAINS A REGIONRESPONSIBLE FOR RESISTANCE TO ANTIVIRAL EFFECTS OF INTERFERON/, Journal of General Virology, 79, 1998, pp. 565-572
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.