pH mediated inhibition of the cell to cell spread of herpes simplex virus infection.
The relationships between the environmental pH and the replication and spread of herps simplex virus (HSV) infection in rabbit skin (RS) cell cultures was studies. Relative to the plaque formation at pH7.0, incubation of RS cells with medium adjusted to pH 6.6 resulted in a 50 to 70 per cent decrement in plaque number. The addition of overlay media adjusted to pH 6.0 or 6.3 precluded HSV plaque formation. Select HSV-1 (type 1) and HSV (type 2) strains readily survived a 3 day incubation with medium adjusted to pH 6.3 as demonstrated by plaque production following a medium shift to pH 7.0. Rs cells incubated with medium at pH 6.3 did not replicate. The survival of RS cells incubated for 3 days with medium adjusted to pH 6.3 was demonstrated by renewed cell proliferation following a medium change from pH 6.3 to 7.0. The progeny virus yields of two HSV strains replicating in RS cells incubated with medium adjusted to pH 6.3 or 7.0 were equivalent at 24 or 48 hours post infection and were indicative of a productive infection. The inhibition of HSV plaque formation at pH 6.3 was not due to an alteration of cell receptors but was the result of an inhibition in the cell to cell spread of the virus. These results are discussed with regard to the possibility that the decline in pH associated with the inflammatory response may serve as a host defense against HSV infections.
pH mediated inhibition of the cell to cell spread of herpes simplex virus infection. The relationships between the environmental pH and the replication and spread of herps simplex virus (HSV) infection in rabbit skin (RS) cell cultures was studies. Relative to the plaque formation at pH7.0, incubation of RS cells with medium adjusted to pH 6.6 resulted in a 50 to 70 per cent decrement in plaque number. The addition of overlay media adjusted to pH 6.0 or 6.3 precluded HSV plaque formation. Select HSV-1 (type 1) and HSV (type 2) strains readily survived a 3 day incubation with medium adjusted to pH 6.3 as demonstrated by plaque production following a medium shift to pH 7.0. Rs cells incubated with medium at pH 6.3 did not replicate. The survival of RS cells incubated for 3 days with medium adjusted to pH 6.3 was demonstrated by renewed cell proliferation following a medium change from pH 6.3 to 7.0. The progeny virus yields of two HSV strains replicating in RS cells incubated with medium adjusted to pH 6.3 or 7.0 were equivalent at 24 or 48 hours post infection and were indicative of a productive infection. The inhibition of HSV plaque formation at pH 6.3 was not due to an alteration of cell receptors but was the result of an inhibition in the cell to cell spread of the virus. These results are discussed with regard to the possibility that the decline in pH associated with the inflammatory response may serve as a host defense against HSV infections.