The virion host shutoff function of herpes simplex virus type 1 plays a role in corneal invasion and functions independently of the cell cycle.
A significant restriction was demonstrated in the ability of herpes simplex virus type 1 virion host shutoff (vhs) mutant viruses to invade the corneal epithelium. Viral replication and invasion was confined to the areas of the cornea which were scarified prior to infection. Differences between wild-type and vhs mutant replication in corneas in vivo were 100- to 1000-fold at all timepoints postinfection. Smaller but still significant growth restrictions were observed in cultured corneal cells. This difference between in vitro and in vivo is not likely to be due to differences in cell cycle status since vhs-induced RNA degradation can occur in both cycling and noncycling cells in vitro. The vhs function is therefore important for invasion of the cornea and secondarily the nervous system and is thereby required for efficient establishment of latency.
Strelow
L
L
Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Smith
T
T
Leib
D
D
D000818:Animals; D002453:Cell Cycle; D002478:Cells, Cultured; D002522:Chlorocebus aethiops; D003315:Cornea / Q000166:cytology / Q000821:virology; D005260:Female; D018259:Herpesvirus 1, Human / Q000254:growth & development / Q000502:physiology*; D006801:Humans; D016849:Keratitis, Herpetic / Q000821:virology*; D051379:Mice; D012260:Ribonucleases; D014709:Vero Cells; D014764:Viral Proteins / Q000235:genetics / Q000502:physiology*; D014779:Virus Replication
D014764:Viral Proteins; C070722:virion host shutoff protein, Simplexvirus; D012260:Ribonucleases