title: US3 protein kinase of herpes simplex virus protects primary afferent neurons from virus-induced apoptosis in ICR mice.
abstract: Possible roles of the US3 gene of the herpes simplex virus (HSV) in the interaction between the virus and primary afferent neurons were examined. Neuronal apoptosis was observed in the trigeminal ganglion of mice that were infected with the wild-type (wt) of HSV-2 strain 186 and with US3-deficient mutant virus (L1BR1). In wt virus-infected mice, many HSV-immunoreactive (HSV-ir) cells were seen throughout the trigeminal ganglion, although no apoptotic change was detected. On the other hand, HSV-ir cells in L1BR1-infected mice were found only in the ophthalmic division of the trigeminal ganglions. Examination by HSV-immunohistochemistry combined with the terminal deoxynucleotidal transferase (Tdt)-mediated deoxyuridin 5'-triphosphate (dUTP) nick-end labeling (TUNEL) method showed that DNA fragmentation had occurred in almost all HSV-ir cells in the L1BRI-infected ganglion. Ultrastructurally, many viral particles were detected in apoptotic ganglionic neurons of mice infected with L1BR1. These results indicate that US3 protein kinase (US3pk) played a role in protecting HSV-infected primary afferent neurons from apoptotic cell death. The present study suggests that US3pk plays a role when HSV establishes latent infections in the sensory ganglia.
authors.affiliation: Department of Ophthalmology, Research Institute for Disease Mechanism and Control, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, 466-8550, Nagoya, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Asano
authors.forename: T
authors.initials: T
authors.lastname: Honda
authors.forename: F
authors.initials: F
authors.lastname: Goshima
authors.forename: Y
authors.initials: Y
authors.lastname: Nishiyama
authors.forename: Y
authors.initials: Y
authors.lastname: Sugiura
mesh_terms: D000818:Animals; D017209:Apoptosis; D003315:Cornea / Q000821:virology; D003588:Cytopathogenic Effect, Viral / Q000235:genetics; D053938:DNA Fragmentation; D018258:Herpesvirus 2, Human / Q000201:enzymology* / Q000235:genetics / Q000472:pathogenicity; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009475:Neurons, Afferent / Q000473:pathology / Q000648:ultrastructure / Q000821:virology*; D017346:Protein Serine-Threonine Kinases / Q000172:deficiency* / Q000235:genetics; D013047:Specific Pathogen-Free Organisms; D012668:Trigeminal Ganglion / Q000473:pathology / Q000648:ultrastructure / Q000821:virology*; D014764:Viral Proteins; D017735:Virus Latency / Q000235:genetics
chemical_list: D014764:Viral Proteins; D017346:Protein Serine-Threonine Kinases; C084395:US3 protein, Human herpesvirus 2