Skip Navigation

This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow References
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Request Permissions
Google Scholar
Right arrow Articles by Liu, P.
Right arrow Articles by Nian, M.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Liu, P.
Right arrow Articles by Nian, M.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?


Molecular pathophysiological mechanisms in virus infected host myocardium

P. Liu1,1,2, P. Lee1,2, K. Fuse3 and M. Nian1,2

a Heart & Stroke/Richard Lewar Centre of Excellence, University of Toronto, Toronto, Ontario, Canada
b Toronto General Hospital, University Health Network, Toronto, Ontario, Canada
c Niigata University, Niigata, Japan

1 Correspondence: Dr. Peter Liu (Heart & Stroke/Polo Chair Professor of Medicine at the University of Toronto), Heart & Stroke/RL Centre of Excellence, EN12-324, Toronto General Hospital, 200 Elizabeth Street, Toronto, Ontario, M5G 2C4, Canada.

Abstract

The pathophysiological mechanisms of viral myocarditis are now better understood. The coxsackieviral receptors coxsackie adenoviral receptor (CAR) and decay accelerating factor (DAF) are linked to immune activation signalling pathways such as tyrosine kinase p56lck. Viral infection in murine knockout models has permitted identification of the mutually facilitatory roles of CD4 and CD8, which control the cytokine profile and the T-helper-1 versus T-helper-2 repertoire. The T-cell receptor associated tyrosine kinase p56lck is critical for disease progression, as in its absence the host will achieve 100% survival with limited viral replication. The major downstream target from p56lck is extracellular signal-related receptor , which is responsible for cytokine production in T cells and for viral proliferation in the host tissues. Finally, the system is modulated by the tyrosine phosphatase CD45. Recent investigations have provided an enriched environment from which to select future targets for intervention in the clinical arena, and have allowed expansion of these concepts to other types of heart failure.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.