Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

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

DOI

10.1006/viro.1996.0141

Type

Journal article

Journal

Virology

Publication Date

03/1996

Volume

217

Pages

470 - 477

Addresses

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

Keywords

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