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