Virus-induced neuronal apoptosis blocked by the herpes simplex virus latency-associated transcript.
Latent infections with periodic reactivation are a common outcome after acute infection with many viruses. The latency-associated transcript (LAT) gene is required for wild-type reactivation of herpes simplex virus (HSV). However, the underlying mechanisms remain unclear. In rabbit trigeminal ganglia, extensive apoptosis occurred with LAT(-) virus but not with LAT(+) viruses. In addition, a plasmid expressing LAT blocked apoptosis in cultured cells. Thus, LAT promotes neuronal survival after HSV-1 infection by reducing apoptosis.
Perng
G C
GC
Ophthalmology Research Laboratories, Cedars-Sinai Medical Center Burns & Allen Research Institute, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA.
Jones
C
C
Ciacci-Zanella
J
J
Stone
M
M
Henderson
G
G
Yukht
A
A
Slanina
S M
SM
Hofman
F M
FM
Ghiasi
H
H
Nesburn
A B
AB
Wechsler
S L
SL
D000818:Animals; D017209:Apoptosis; D002460:Cell Line; D005814:Genes, Viral; D018259:Herpesvirus 1, Human / Q000235:genetics / Q000502:physiology*; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D016849:Keratitis, Herpetic / Q000473:pathology* / Q000821:virology*; D009154:Mutation; D009474:Neurons / Q000473:pathology* / Q000821:virology; D011065:Poly(ADP-ribose) Polymerases / Q000276:immunology / Q000378:metabolism; D011817:Rabbits; D014158:Transcription, Genetic; D012668:Trigeminal Ganglion / Q000473:pathology / Q000821:virology; D014775:Virus Activation; D017735:Virus Latency / Q000235:genetics*
D011065:Poly(ADP-ribose) Polymerases