We provide evidence that (i) variants lacking individual herpes simplex virus type 1 (HSV-1) I sites can be selected following extensive I treatment of the viral DNA and can be recombined to produce HSV-1 variants lacking two of the four sites normally found, (ii) all I sites can be removed from a viable intertypic recombinant HSV genome, (iii) following I treatment, different mutants with deletions (0.15 to 8.8 kb) in the long repeat (TR or IR) and long unique regions can be readily isolated, as well as mutants with novel I sites, (iv) several mutants with deletions in one of the repeats (TR or IR) have a measurable growth disadvantage in tissue culture.

Keyword(s): deletion mutants , HSV-1 and XbaI

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