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Recent reports have highlighted a potential antiviral activity for nitric oxide (NO). The purpose of this study was to investigate the production of NO in mice during vaccinia virus (VV) or herpes simplex virus type 1 infection, and to assess the role of NO in clearance of VV. Reactive nitrogen intermediates (RNI; NO and its stable oxidation products, nitrite and nitrate) were significantly elevated in the plasma of mice infected with these viruses. Furthermore, spleen cells from virus-infected mice produced elevated RNI levels following stimulation in vitro with LPS. NO production during VV infection was critically dependent on the cytokines tumor necrosis factor and interferon-gamma, and on the presence of both CD4+ and CD8+ T lymphocytes. Treatment of VV-infected mice with the nitric oxide synthase inhibitor N(G)-methyl-L-arginine did not alter the course of infection, suggesting that NO may not be essential for the clearance of this virus.

Original publication




Journal article



Publication Date





470 - 477


Division of Cell Biology, John Curtin School of Medical Research, Canberra, Australia.


Spleen, CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, Cells, Cultured, Animals, Mice, Inbred C57BL, Mice, Inbred CBA, Mice, Ectromelia virus, Vaccinia virus, Ectromelia, Infectious, Vaccinia, Nitric Oxide, Tumor Necrosis Factor-alpha, Female, Nitric Oxide Synthase, Interferon-gamma