AI Article Synopsis
- Infections play a significant role in various heart diseases, particularly emphasizing the link between Coxsackievirus B3 (CVB3) and chronic dilated cardiomyopathy, which can lead to severe health issues like heart failure.
- Research indicates that the Src family kinase Lck (p56lck) is crucial for effective CVB3 replication in T-cells and for sustained viral activity in living organisms.
- Mice without the p56lck gene showed complete protection against severe health effects from CVB3, highlighting its essential role in viral replication and pathogenicity in heart disease.
Article Abstract
Infections are thought to be important in the pathogenesis of many heart diseases. Coxsackievirus B3 (CVB3) has been linked to chronic dilated cardiomyopathy, a common cause of progressive heart disease, heart failure and sudden death. We show here that the sarcoma (Src) family kinase Lck (p56lck) is required for efficient CVB3 replication in T-cell lines and for viral replication and persistence in vivo. Whereas infection of wild-type mice with human pathogenic CVB3 caused acute and very severe myocarditis, meningitis, hepatitis, pancreatitis and dilated cardiomyopathy, mice lacking the p56lck gene were completely protected from CVB3-induced acute pathogenicity and chronic heart disease. These data identify a previously unknown function of Src family kinases and indicate that p56lck is the essential host factor that controls the replication and pathogenicity of CVB3.
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