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.
Nichol
P F
PF
Department Internal Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.
Chang
J Y
JY
Johnson
E M
EM
Olivo
P D
PD
D000818:Animals; D002478:Cells, Cultured; D006561:Herpes Simplex / Q000378:metabolism*; D007150:Immunohistochemistry; D009475:Neurons, Afferent / Q000821:virology*; D016716:PC12 Cells; D014176:Protein Biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D018139:Simplexvirus / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000821:virology*