Protective role for interferon-beta in coxsackievirus B3 infection

Article

关键词: INDUCED MYOCARDITIS;    HEART-DISEASE;    REPLICATION;    ALPHA;    MICE;    VIRUSES;    CELLS;    RNA;   

DOI  :  10.1161/01.CIR.0000136824.73458.20

来源: SCIE

【 摘 要 】

Background - 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.

【 授权许可】

Free