Functions and proteins of herpes simplex virus type-1 that are involved in raising the mutation frequency of infected cells

Abstract

When cells are infected by herpes simplex virus type-1 (HSV-1) the mutation frequency is increased. To find which functions of the virus are responsible for this, a variety of viral strains and one fragment of viral DNA were tested in a mutagenesis assay. Mutagenesis was dependent on the binding of the virus to the cell surface and disassembly of the virus particle, but expression of virus genes was not necessary. Since this implied that mutagenesis was a result of the exposure of the interior of the cell to an internal structural component of the virus, the role of two likely components was examined. The host-shutoff function of the virus was not required for mutagenesis. However, a fragment of DNA from within the minimum transforming region of HSV-1 that encodes a possible virion protein was mutagenic when expressed from a eukaryotic expression vector. The encoded product of this DNA fragment is therefore a candidate for a transforming protein of HSV-1, and is the only protein currently suggested to be responsible for that function.