Mice lacking inducible nitric-oxide synthase are more susceptible to herpes simplex virus infection despite enhanced Th1 cell responses.

Abstract

Mice deficient in the inducible nitric-oxide synthase (iNOS), constructed by gene-targeting, were significantly more susceptible to herpes simplex virus (HSV)-1 infection, displayed a delayed clearance of virus from the dorsal root ganglia (DRG) and exhibited an increase in the frequency of virus reactivation in DRG compared with similarly infected heterozygous mice. The infected iNOS-deficient mice developed enhanced Th1-type immune responses and their spleen cells produced higher concentrations of IL-12 than similarly infected heterozygous mice. This finding suggests that iNOS plays an important role in resistance against HSV-1 infection. Furthermore, nitric oxide (NO) may block the development of Th1 cells via inhibition of IL-12 synthesis and thereby play a role in immune regulation.

• Authors: A MacLean, X Q Wei, F P Huang, U A Al-Alem, W L Chan, F Y Liew
• Journal: The Journal of general virology (J Gen Virol) Vol. 79 ( Pt 4) Pg. 825-30 (Apr 1998) ISSN: 0022-1317 [Print] England
• PMID: 9568978 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Interleukin-12
• Nitric Oxide
• Nitric Oxide Synthase
• Nitric Oxide Synthase Type II
• Nos2 protein, mouse

Topics

• Animals
• Female
• Ganglia, Spinal (virology)
• Herpes Simplex (enzymology, etiology, immunology)
• Herpesvirus 1, Human (immunology, isolation & purification, pathogenicity)
• Heterozygote
• Homozygote
• Interleukin-12 (biosynthesis)
• Male
• Mice
• Mice, Knockout
• Nitric Oxide (immunology)
• Nitric Oxide Synthase (deficiency, genetics, immunology)
• Nitric Oxide Synthase Type II
• Th1 Cells (immunology)