A hamster cell line (HDC-22) developed in our laboratory was non-permissive for herpes simplex virus type 2 (HSV-2) but not for herpes simplex virus type 1 (HSV-1). The mechanism of resistance to productive infection by HSV-2 was investigated. Adsorption studies revealed that HSV-1 and HSV-2 adsorbed at similar rates to the HDC-22 cells. The HDC-22 cells, when infected with HSV-2, produced minimal amounts of virus-specific antigens which increased slightly after several days.

The amount of HSV-2 DNA produced in the HDC-22 cells was always less than when these cells were infected with HSV-1. Cellular DNA synthesis was severely depressed by infection with HSV-1 at a multiplicity of 1 while HSV-2 had no effect at this multiplicity. At a higher multiplicity (of 5), this effect was increased with HSV-1 and noticeable with HSV-2. These studies indicate that the block for infection of the HDC-22 cell line with HSV-2 is after virus adsorption and may involve synthesis of virus DNA.


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