Failure of intertypic complementation and recombination between non-fusing mutants of herpes simplex virus. Types 1 and 2.

Abstract

Mixed infections of cells with pairs of r mutants (mutants defective in fusion function) of herpes simplex virus types 1 and 2 resulted in the cytopathic change of cell rounding (no complementation) and did not pro duce the recombinant, which formed a large syncytium due to cell fusion (no recombination). No complementation was observed in the superinfection after various times with heterologous r mutant and also in mixed infections with three r mutants, two belonging to separate complementation groups of one type and one of the opposite type. These observations led to the hypothesis that some gene (s) involved in r mutant and in fusion-causing virus encode an inhibitory factor against cell fusion caused by the heterologous type virus.