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Cardiovascular Research Advance Access first published online on July 3, 2009
This version [Corrected Proof] published online on August 6, 2009
Cardiovascular Research, doi:10.1093/cvr/cvp225
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

Protein degradation systems in viral myocarditis leading to dilated cardiomyopathy

Honglin Luo*, Jerry Wong and Brian Wong

Department of Pathology and Laboratory Medicine, The James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, Providence Heart+Lung Institute, St. Paul's Hospital-University of British Columbia, 1081 Burrard Street, Vancouver, BC, Canada V6Z 1Y6

* Corresponding author. Tel: +1 604 682 2344; fax: +1 604 806 8351. E-mail address: hluo{at}mrl.ubc.ca

The primary intracellular protein degradation systems, including the ubiquitin-proteasome and the lysosome pathways, have been emerging as central regulators of viral infectivity, inflammation, and viral pathogenicity. Viral myocarditis is an inflammatory disease of the myocardium caused by virus infection in the heart. The disease progression of viral myocarditis occurs in three distinct stages: acute viral infection, immune cell infiltration, and cardiac remodelling. Growing evidence suggests a crucial role for host proteolytic machineries in the regulation of the pathogenesis and progression of viral myocarditis in all three stages. Cardiotropic viruses evolve different strategies to subvert host protein degradation systems to achieve successful viral replication. In addition, these proteolytic systems play important roles in the activation of innate and adaptive immune responses during viral infection. Recent evidence also suggests a key role for the ubiquitin-proteasome and lysosome systems as the primary effectors of protein quality control in the regulation of cardiac remodelling. This review summarizes the recent advances in understanding the direct interaction between cardiotropic viruses and host proteolytic systems, with an emphasis on coxsackievirus B3, one of the primary aetiological agents causing viral myocarditis, and highlights possible roles of the host degradation systems in the pathogenesis of viral myocarditis and its progression to dilated cardiomyopathy.

KEYWORDS Viral myocarditis; Dilated cardiomyopathy; Coxsackievirus; Proteasome; Immunoproteasome; Autophagy; Autophagosome; Proteasome activators

Time for primary review: 25 days

This article is part of the Spotlight Issue on: The Role of the Ubiquitin-Proteasome Pathway in Cardiovascular Disease


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