Interferon-gamma induced type I nitric oxide synthase activity inhibits viral replication in neurons.
Type I NOS expression increases in OB neurons during VSV infection. Immunocytochemical staining of NB41A3 cells indicates constitutive expression of interferon (IFN)-gamma receptor and type I NOS. IFN-gamma treatment of NB41A3 cells increased NO production and type I NOS protein. In vitro replication of VSV, polio virus type I, and Herpes Simplex virus type I (HSV-1) is significantly inhibited by IFN-gamma induced type I NOS and antagonized by NOS inhibitors. In contrast, while IFN-gamma 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-gamma induced type I NOS activity may play an important role in host immunity against neurotropic viral infections.[1]References
- Interferon-gamma induced type I nitric oxide synthase activity inhibits viral replication in neurons. Komatsu, T., Bi, Z., Reiss, C.S. J. Neuroimmunol. (1996) [Pubmed]
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