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(Circulation Research. 2006;99:346.)
© 2006 American Heart Association, Inc.

Editorials

Integrin-Linked Kinase Plays a Key Role in Coxsackievirus Replication

Charles J. Lowenstein

From the Department of Medicine and Pathology, The Johns Hopkins University School of Medicine, Baltimore, Md.

Correspondence to Charles J. Lowenstein, 950 Ross Building, 720 Rutland Ave, The Johns Hopkins University School of Medicine, Baltimore, MD 21205. E-mail clowenst@jhmi.edu

See related article, pages 354–361

Key Words: ILK • Coxsackievirus • Akt signaling • decay accelerating factor • apoptosis

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Viral infection may be a major cause of idiopathic dilated cardiomyopathy, but little is known about how viruses enter the cardiac myocyte and damage it. Understanding the pathogenesis of viral myocarditis will lead to new strategies for the treatment and prevention of heart failure. In this issue of Circulation Research, Esfandiareiet al show that the integrin-linked kinase (ILK) plays a key role in the lifecycle of the cardiotropic virus Coxsackievirus.¹

More than 100 000 patients in the United States have a nonischemic dilated cardiomyopathy, and this disease accounts for 45% of all heart transplants.^2,3 More than 25% of the nonischemic dilated cardiomyopathy cases may be caused by viral infections.⁴ The virus that most commonly infects the heart is Coxsackievirus, a small RNA virus (picornavirus) spread through the fecal–oral route.⁵ Coxsackievirus infection causes a viral prodrome of fever and myalgias, followed by diarrhea. Approximately 2 weeks after the onset of infection, direct viral injury of cardiac myocytes in combination with the inflammatory host response cause a cardiomyopathy. The clinical course of viral cardiomyopathy is highly variable, ranging from an acute fulminant disease, with complete recovery, to a smoldering chronic inflammatory state with progressive heart failure and death.

The lifecycle of Coxsackievirus is short and simple. Coxsackievirus binds to 2 receptors, decay accelerating factor (DAF) and the Coxsackievirus adenovirus receptor (CAR), and then enters the cardiac myocyte.⁶ The virus hijacks the host, forcing it to translate its RNA genome into a single large polyprotein. Viral proteases then cleave this polyprotein into . . . [Full Text of this Article]

Related Article:

Novel Role for Integrin-Linked Kinase in Modulation of Coxsackievirus B3 Replication and Virus-Induced Cardiomyocyte Injury

Mitra Esfandiarei, Agripina Suarez, Ansel Amaral, Xiaoning Si, Maziar Rahmani, Shoukat Dedhar, and Bruce M. McManus
Circ. Res. 2006 99: 354-361. [Abstract] [Full Text] [PDF]