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Protective role for interferon-beta in coxsackievirus B3 infection.

AbstractBACKGROUND:
Coxsackievirus-induced myocarditis can be a serious cause of heart failure. In the absence of a specific antiviral therapy, modulating the host immune response may be protective. Interferons (IFNs)-alpha and -beta perform a fundamental role in innate and adaptive antiviral responses, thereby presenting as candidate therapeutics for coxsackievirus infections.
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.
AuthorsRaj Deonarain, Dante Cerullo, Koichi Fuse, Peter P Liu, Eleanor N Fish
JournalCirculation (Circulation) Vol. 110 Issue 23 Pg. 3540-3 (Dec 07 2004) ISSN: 1524-4539 [Electronic] United States
PMID15249500 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Interferon-alpha
  • Interferon-beta
  • Protein Serine-Threonine Kinases
  • 2',5'-Oligoadenylate Synthetase
  • GTP Phosphohydrolases
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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