1887

Abstract

Double infection with two interferon (IFN)-sensitive strains of herpes simplex virus (HSV), HSV-1(17syn) and HSV-2(UW268), showed reduced inhibition of virus growth by IFN. Intertypic recombinants with IFN resistance were obtained from the doubly infected cultures. These results indicate that HSV IFN resistance is controlled by at least two genetic regions. Restriction endonuclease analysis demonstrated that the recombinants were similar to HSV-2 in their genomic structure but the HI-A, II-I and II-N fragments of HSV-2 were commonly lost in the recombinants, suggesting that any of these fragments could be associated with HSV-2 IFN resistance. We cloned these fragments and HI-E, which overlaps II-N, from an IFN-resistant HSV-2 strain, HSV-2(G), and examined each fragment for its ability to rescue IFN resistance of HSV- 2(UW268) by co-transfecting with the HSV- 2(UW268) genome. Of the HSV-2(G) fragments, only II-N increased plating efficiency of progeny viruses in IFN-treated cells. An IFN-resistant HSV-2 clone was obtained from the II-N of HSV-2(G) and HSV-2(UW268) genome co-transfected culture, and a part of II-N of HSV-2(UW268) was replaced with that 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 II-N fragment of HSV-2.

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1998-03-01
2021-10-19
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