Infection of sympathetic and sensory neurones with herpes simplex virus does not elicit a shut-off of cellular protein synthesis: implications for viral latency and herpes vectors.

Infection of non-neuronal cell types with herpes simplex virus type 1 (HSV-1) results in the degradation of host mRNA (Kwong & Frenkel 1987) and a shutoff in host protein synthesis (Roizman et al. 1965). This effect is mediated by a virion associated protein that is encoded by the viral vhs gene (Read & Frenkel 1983). This virion host shutoff (VHS) helps regulate viral gene expression and promotes efficient viral replication during the lytic cycle (Kwong & Frenkel 1987). Cultured sympathetic and sensory neurones, in contrast to primary rat fibroblasts, PC-12 cells, and Vero cells, showed no reduction in protein synthesis following infection with HSV-1. The resistance of neurones to VHS may be important in allowing establishment of a latent infection. In addition, this finding has a favourable impact on the idea of using HSV as a vector to deliver foreign genes into neurones.