Table 4.
Viral infection in which pathogenesis/protection is through NO production *
Virus | Test system | Site/lesion | Mechanisms of NO production | References |
---|---|---|---|---|
NO‐mediated pathology | ||||
Rotavirus | Mice in vivo; ex vivo ileal loop | Ileum/diarrhoea | Upregulation of ileal iNOS mRNA by virus and by NS4 protein | Borghan et al. (2007) |
Coxsackie B | Mice | Myocarditis | Increased iNOS/NO | Bevan et al. (2001) |
Herpes simplex 1 | Mice | Liver/apoptosis | Increased production of NO, TNF‐α, IL‐6, IFN‐γ | Irie & Shiga (2005) |
HIV | Cortical cell culture | Neurotoxicity | Activation of NOS by HIVgp120 and cytokines | Dawson et al. (1993) |
PBMC monocyte | Lymphocyte inactivation | Large amount of NO production | Groeneveld et al. (1996) | |
Cardiomyocyte culture, animals | Cardiomyopathy | NO induced cardiomyocyte apoptosis by TNF type 1 receptor activation | Monsuez et al. (2007) | |
Microglia cells | Neurodegeneration | NO‐induced oxidative stress | Roy et al. (2008) | |
Influenza A | Mice | Pneumonitis | iNOS presence | Karupiah et al. (1998) |
Tick‐borne encephalitis virus | Mice | Encephalitis | Increased NO | Kreil & Eibl (1996) |
Adenovirus | Mice | Lung inflammation | iNOS and peroxynitrite‐generated nitrotyrosine | Zsengellér et al. (2001) |
Murine cytomegalovirus | Mice | Pneumonitis | Increased NO | Tanaka et al. (1997) |
Hepatitis C | Hepatocyte culture | Hepatitis, oncogenesis | Increased iNOS/NO | Machida et al. (2004) |
NO‐mediated protection of pathology | ||||
Japanese encephalitis | Mice | Encephalitis protected | Production of macrophage‐derived neutrophil chemotactic factor increases iNOS | Saxena et al. (2001) |
Junín virus | Mice, astrocyte culture | Brain damage protected | INOS inhibition increases brain damage | Gómez et al. (2003) |
Only a few examples have been cited.