title: Corneal infection of herpes simplex virus type 2--induced neuronal apoptosis in the brain stem of mice with expression of tumor suppressor gene (p53) and transcription factors.
abstract: To understand the mechanism of neuronal apoptosis induced by herpes simplex virus (HSV) infection in vivo, the distribution of viral antigen, the appearance of apoptotic bodies, and the expressions of the tumor suppressor gene p53 and several transcription factors such as c-fos, c-jun and NF-kappaB were examined immunohistochemically and histopathologically after corneal infection of mice with HSV type 2 strain 186. Five days after HSV infection, viral antigen was diffusely detected in the corneal epithelium, the trigeminal ganglion and the pars caudalis of the spinal trigeminal nucleus. Neuronal apoptosis was observed in the brain stem ipsilateral to the HSV-infected side with the immunoreactivities of c-fos, c-jun, NF-kappaB and p53. Dual-labeling immunohistochemical studies revealed that almost all of the viral antigen-positive neurons and glia in the brain stem also showed p53 immunoreactivity. On the other hand, no neuronal apoptosis but only with the expression of c-jun was found in the trigeminal ganglion. Our results suggest that the different expression of transcription factors between the brain stem and the trigeminal ganglion may influence the neuronal apoptosis induced by HSV infection.
authors.affiliation: Laboratory of Virology, Research Institute of Disease Mechanism and Control, Nagoya University School of Medicine, Aichi, Japan.
authors.forename: D
authors.initials: D
authors.lastname: Watanabe
authors.forename: T
authors.initials: T
authors.lastname: Honda
authors.forename: K
authors.initials: K
authors.lastname: Nishio
authors.forename: Y
authors.initials: Y
authors.lastname: Tomita
authors.forename: Y
authors.initials: Y
authors.lastname: Sugiura
authors.forename: Y
authors.initials: Y
authors.lastname: Nishiyama
mesh_terms: D000344:Afferent Pathways / Q000378:metabolism / Q000473:pathology / Q000821:virology; D000818:Animals; D017209:Apoptosis / Q000235:genetics*; D001933:Brain Stem / Q000378:metabolism / Q000473:pathology / Q000821:virology*; D015740:Calcitonin Gene-Related Peptide / Q000378:metabolism; D002452:Cell Count; D048429:Cell Size / Q000502:physiology; D003315:Cornea / Q000473:pathology / Q000503:physiopathology / Q000821:virology; D020803:Encephalitis, Herpes Simplex / Q000235:genetics* / Q000473:pathology / Q000503:physiopathology; D015967:Gene Expression Regulation, Viral / Q000502:physiology; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009410:Nerve Degeneration / Q000235:genetics / Q000473:pathology / Q000821:virology; D009474:Neurons / Q000378:metabolism / Q000473:pathology / Q000821:virology*; D018139:Simplexvirus / Q000235:genetics* / Q000378:metabolism / Q000472:pathogenicity; D014157:Transcription Factors / Q000502:physiology*; D014275:Trigeminal Caudal Nucleus / Q000378:metabolism / Q000473:pathology / Q000821:virology; D012668:Trigeminal Ganglion / Q000378:metabolism / Q000473:pathology / Q000821:virology; D016159:Tumor Suppressor Protein p53 / Q000235:genetics*
chemical_list: D014157:Transcription Factors; D016159:Tumor Suppressor Protein p53; D015740:Calcitonin Gene-Related Peptide