Nitric oxide and Coxsackievirus B3 myocarditis: Differential expression of inducible nitric oxide synthase in mouse heart after infection with virulent or attenuated virus
| Autor: | Hongyi Zhang, Yanwen Li, Leonard C. Archard, Adrian L. Bevan |
|---|---|
| Rok vydání: | 2001 |
| Předmět: |
Male
Myocarditis Guanosine Monophosphate Nitric Oxide Synthase Type II Inflammation Coxsackievirus Virus Nitric oxide Mice chemistry.chemical_compound Virology medicine Animals Cytotoxic T cell Enterovirus Nitrates biology Myocardium Nucleic Acid Hybridization Heart biology.organism_classification medicine.disease Immunohistochemistry Nitric oxide synthase Disease Models Animal Infectious Diseases chemistry biology.protein RNA Viral Tyrosine Nitric Oxide Synthase medicine.symptom Peroxynitrite |
| Zdroj: | Journal of Medical Virology. 64:175-182 |
| ISSN: | 1096-9071 0146-6615 |
| DOI: | 10.1002/jmv.1033 |
| Popis: | Increased expression of inducible nitric oxide synthase (iNOS) has been found in inflammatory myocardial disease and increased production of nitric oxide (NO) has both an inhibitory effect on virus replication and a cytotoxic effect on host cells. To investigate the relationship between severity of enteroviral myocarditis and iNOS expression, a characterised murine model was infected with either cardiovirulent or an attenuated Coxsackievirus B3 and myocardial samples were collected on Day 7. The ability of these viruses to induce NOS expression was compared by measurement of iNOS enzyme activity and localisation of iNOS protein or peroxynitrite, a product of excessive NO production. In accordance with previous reports, high expression of iNOS was detected in mice infected with the cardiovirulent virus. The iNOS protein was located mainly in infiltrating macrophages in and around foci of necrotic myofibres where viral genomic RNA was detected. In contrast, the level of iNOS expression was significantly lower in mice infected with the attenuated virus. This correlates with fewer and smaller myocarditic lesions and less infiltrating cells in the heart. iNOS was not detected in mock-infected mice by the above assays. These findings suggest that one mechanism of attenuation may be associated with the reduced ability of the variant to induce NOS expression in the heart. This also confirms a cytotoxic role for NO in the pathogenesis of Coxsackievirus B3-induced myocarditis. |
| Databáze: | OpenAIRE |
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