Abstract | BACKGROUND: METHODS AND RESULTS: To examine the contribution of IFN-beta in protection from coxsackievirus B3 (CVB3) infection, mice lacking the IFN-beta gene were infected with 10(3) plaque-forming units of CVB3. In contrast to wild-type mice that exhibit an intact IFN-beta response, we observed increased susceptibility to infection (70% mortality), a downregulation of IFN-stimulated gene targets ( 2'-5' oligoadenylate synthetase, serine/threonine protein kinase, the GTPase Mx), and cardiomyocyte breakdown and disruption in the IFN-beta-/- mice. CONCLUSIONS: Viewed together, these results clearly demonstrate that IFN-beta is important in mediating protection against CVB3-induced myocarditis.
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Authors | Raj Deonarain, Dante Cerullo, Koichi Fuse, Peter P Liu, Eleanor N Fish |
Journal | Circulation
(Circulation)
Vol. 110
Issue 23
Pg. 3540-3
(Dec 07 2004)
ISSN: 1524-4539 [Electronic] United States |
PMID | 15249500
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Interferon-alpha
- Interferon-beta
- Protein Serine-Threonine Kinases
- 2',5'-Oligoadenylate Synthetase
- GTP Phosphohydrolases
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Topics |
- 2',5'-Oligoadenylate Synthetase
(biosynthesis)
- Animals
- Coxsackievirus Infections
(immunology, pathology, virology)
- Down-Regulation
- Enterovirus B, Human
- GTP Phosphohydrolases
(biosynthesis)
- Interferon-alpha
(physiology)
- Interferon-beta
(genetics, physiology)
- Mice
- Mice, Knockout
- Myocarditis
(immunology, pathology, virology)
- Myocardium
(pathology)
- Myocytes, Cardiac
(pathology, virology)
- Necrosis
- Protein Serine-Threonine Kinases
(biosynthesis)
- Reverse Transcriptase Polymerase Chain Reaction
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