Genetic studies of cell fusion induced by herpes simplex virus type 1

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Abstract
Eight cell fusion-causing syn mutants were isolated from the KOS strain of herpes simplex virus type 1. Unlike wild-type virus, mutants produced plaques containing multinucleated cells or syncytia. Fusion kinetics curves were established with a Coulter Counter assay for the mutants and wild-type virus in single infections of human embryonic lung cells, for the mutants and wild-type virus in mixed infections (dominance test) and for pairs of mutants in mixed infections (complementation test). In single infections, fusion began 4-6 h after infection and proceeded with an exponential decrease in the number of small single cells. At some later time that was characteristic of the mutant, there was a significant reduction in the rate of fusion for all but possibly one of the mutants. Although the wild-type virus did not produce syncytial plaques, it induced a small amount of fusion that stopped abruptly about 2 h after it started. Thus mutants and wild type induce an active fusion inducer and the activity of this inducer is subsequently inhibited. The extent of fusion is apparently determined by the length of the interval during which the fusion inducer is active. That fusion is actively inhibited in wild-type infections is indicated by syn mutant-infected cells being fused more readily with uninfected cells than with wild type-infected cells. Fusion was decreased in mixed infections with the mutants and wild-type virus but the mutants displayed a codominant fusion phenotype. Fusion was not decreased in mixed infection with pairs of mutants, indicating that the mutants, with one possible exception, are members of the same complementation group. A linkage map was established for 6 mutants by analysis of recombination frequencies.

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