Protective role for interferon-β in coxsackievirus B3 infection
R Deonarain, D Cerullo, K Fuse, PP Liu, EN Fish - Circulation, 2004 - Am Heart Assoc
R Deonarain, D Cerullo, K Fuse, PP Liu, EN Fish
Circulation, 2004•Am Heart AssocBackground—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)-α and-β 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-β in protection from
coxsackievirus B3 (CVB3) infection, mice lacking the IFN-β gene were infected with 103 …
the absence of a specific antiviral therapy, modulating the host immune response may be
protective. Interferons (IFNs)-α and-β 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-β in protection from
coxsackievirus B3 (CVB3) infection, mice lacking the IFN-β gene were infected with 103 …
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)-α and -β 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-β in protection from coxsackievirus B3 (CVB3) infection, mice lacking the IFN-β gene were infected with 103 plaque-forming units of CVB3. In contrast to wild-type mice that exhibit an intact IFN-β 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-β−/− mice.
Conclusions— Viewed together, these results clearly demonstrate that IFN-β is important in mediating protection against CVB3-induced myocarditis.
Am Heart Assoc