Interferon-γ induced type I nitric oxide synthase activity inhibits viral replication in neurons

Takashi Komatsu, Zhengbiao Bi, Carol S. Reiss

Research output: Contribution to journalArticle

Abstract

Type I NOS expression increases in OB neurons during VSV infection. Immunocytochemical Staining of NB41A3 cells indicates constitutive expression of interferon (IFN)-γ receptor and type I NOS. IFN-γ treatment of NB41A3 cells increased NO production and type 1 NOS protein. In vitro replication of VSV, polio virus type 1, and Herpes Simplex virus type 1 (HSV-1) is significantly inhibited by IFN-γ induced type I NOS and antagonized by NOS inhibitors. In contrast, while IFN-γ treatment inhibited influenza and Sindbis virus replication, a different pathway(s) was involved. The isoform-selective NOS inhibitor, 7-nitroindazole (7NI) was used to treat mice, resulting in a 10-fold higher titer of virus in brain homogenates, and abrogated the recovery-promoting effect of interleukin-12 treatment. Thus, IFN-γ induced type I NOS activity may play an important role in host immunity against neurotropic viral infections.

Original languageEnglish (US)
Pages (from-to)101-108
Number of pages8
JournalJournal of Neuroimmunology
Volume68
Issue number1-2
DOIs
StatePublished - Aug 1996

Fingerprint

Interferon Type I
Nitric Oxide Synthase
Interferons
Interferon alpha-beta Receptor
Sindbis Virus
Neurons
Human Herpesvirus 1
Poliomyelitis
Virus Diseases
Interleukin-12
Virus Replication
Orthomyxoviridae
Viral Load
Immunity
Protein Isoforms
Staining and Labeling
Viruses
Brain
Infection
Proteins

Keywords

  • Interferon-γ
  • Neuronal nitric oxide synthase
  • Viral infection

ASJC Scopus subject areas

  • Immunology
  • Clinical Neurology
  • Immunology and Allergy
  • Neurology

Cite this

Interferon-γ induced type I nitric oxide synthase activity inhibits viral replication in neurons. / Komatsu, Takashi; Bi, Zhengbiao; Reiss, Carol S.

In: Journal of Neuroimmunology, Vol. 68, No. 1-2, 08.1996, p. 101-108.

Research output: Contribution to journalArticle

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