Co-infection of BS-C-1 cells by the herpes simplex virus type 2 (HSV-2) Curtis strain with its acyclovir (ACV)-resistant mutant (HSV-2-ACV^R), resulted in a severalfold increase in virus yield, as compared to a single infection. On the other hand, when two viruses (G strain and HSV-2-ACV^R) belonging to different strains of HSV-2 were involved, their growth was significantly inhibited; the decrease in the titer of the second virus to infect the cells was greater when its infection took place at later times following infection by the first. This inhibition was not due to the shut-off of host cell protein synthesis caused by the first virus, since an HSV-2 mutant which is unable to inhibit the protein synthesis of the host cell was still capable of efficiently inhibiting the growth of the superinfecting virus.

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