This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Liu, P. P. Articles by Opavsky, M. A. Search for Related Content PubMed PubMed Citation Articles by Liu, P. P. Articles by Opavsky, M. A. Related Collections Structure Other myocardial biology Animal models of human disease Myogenesis

(Circulation Research. 2000;86:253.)
© 2000 American Heart Association, Inc.

Editorials

Viral Myocarditis

Receptors That Bridge the Cardiovascular With the Immune System?

Peter P. Liu, M. Anne Opavsky

From the Heart & Stroke/Lewar Centre of Excellence, University of Toronto, Toronto, Ontario, Canada.

Correspondence to Dr Peter Liu, Heart & Stroke/Lewar Centre of Excellence, EN12-324, 200 Elizabeth St, Toronto, Ontario, Canada M5G 2C4. E-mail peter.liu@utoronto.ca

Key Words: receptors • adenovirus • cardiomyocytes

	Introduction

 
Viral myocarditis exhibits different clinical phenotypes depending on the age of the patient. In pediatric patients, viral myocarditis can present as acute heart failure and cardiogenic shock, and in older patients, it often presents as chronic, slowly progressive heart failure and dilated cardiomyopathy. The severity of viral myocarditis is determined by a delicate balance between the viral infection and the inflammatory response that is engendered in the host.

The commonest viral causes of human myocarditis include coxsackievirus B group and adenovirus. It is no accident that these two viruses emerged as the commonest etiological agent of myocarditis. Recent elegant work by Bergelson et al¹ demonstrated that both of these viruses share a common cell surface receptor—coxsackie-adenoviral receptor (CAR).

CAR is a 46-kDa member of the immunoglobulin (Ig) superfamily, featuring the Ig loops maintained by disulphide bonds between appropriately positioned cysteines. The extracellular domain is the key functional component for coxsackievirus internalization.² CAR also serves as an attachment receptor for adenovirus. However, the natural function and regulation of CAR are still relatively unknown.

The efficiency in targeting the host cell by coxsackievirus and adenovirus depends on their distinct coreceptors. Coxsackievirus B (CVB) uses the complement deflecting protein decay accelerating factor (DAF, CD55) as its coreceptor,³ whereas adenovirus uses integrin _vß₃ and _vß₅ as its coreceptors.⁴ DAF as a coreceptor serves an important function by significantly increasing the binding efficiency of coxsackievirus onto the DAF-CAR receptor complex to facilitate internalization by CAR.⁵

	Role of the Receptors in Viral Myocarditis

 
Myocarditis is both a viral and inflammatory disease. The virus . . . [Full Text of this Article]

This article has been cited by other articles:

				X. Si, H. Luo, A. Morgan, J. Zhang, J. Wong, J. Yuan, M. Esfandiarei, G. Gao, C. Cheung, and B. M. McManus Stress-Activated Protein Kinases Are Involved in Coxsackievirus B3 Viral Progeny Release J. Virol., November 15, 2005; 79(22): 13875 - 13881. [Abstract] [Full Text] [PDF]

				K. Fuse, G. Chan, Y. Liu, P. Gudgeon, M. Husain, M. Chen, W.-C. Yeh, S. Akira, and P. P. Liu Myeloid Differentiation Factor-88 Plays a Crucial Role in the Pathogenesis of Coxsackievirus B3-Induced Myocarditis and Influences Type I Interferon Production Circulation, October 11, 2005; 112(15): 2276 - 2285. [Abstract] [Full Text] [PDF]

				J. W Mason Myocarditis and dilated cardiomyopathy: An inflammatory link Cardiovasc Res, October 15, 2003; 60(1): 5 - 10. [Abstract] [Full Text] [PDF]

				M. Raatikka, P. M. Pelkonen, J. Karjalainen, and E. V. Jokinen Recurrent pericarditis in children and adolescents: Report of 15 cases J. Am. Coll. Cardiol., August 20, 2003; 42(4): 759 - 764. [Abstract] [Full Text] [PDF]

				C. Communal, F. Huq, D. Lebeche, C. Mestel, J. K. Gwathmey, and R. J. Hajjar Decreased Efficiency of Adenovirus-Mediated Gene Transfer in Aging Cardiomyocytes Circulation, March 4, 2003; 107(8): 1170 - 1175. [Abstract] [Full Text] [PDF]

				W. Poller, H. Fechner, M. Noutsias, C. Tschoepe, M. Pauschinger, and H.-P. Schultheiss The molecular basis of cardiotropic viral infections Eur. Heart J. Suppl., December 1, 2002; 4(suppl_I): I18 - I30. [Abstract] [PDF]

				P. Liu, P. Lee, K. Fuse, and M. Nian Molecular pathophysiological mechanisms in virus infected host myocardium Eur. Heart J. Suppl., December 1, 2002; 4(suppl_I): I37 - I41. [Abstract] [PDF]

				T. P. Zwaka, D. Manolov, C. Ozdemir, N. Marx, Z. Kaya, M. Kochs, M. Hoher, V. Hombach, and J. Torzewski Complement and Dilated Cardiomyopathy: A Role of Sublytic Terminal Complement Complex-Induced Tumor Necrosis Factor-{alpha} Synthesis in Cardiac Myocytes Am. J. Pathol., August 1, 2002; 161(2): 449 - 457. [Abstract] [Full Text] [PDF]

				J.M. Hare and K.L. Baughman Fulminant and acute lymphocytic myocarditis: the prognostic value of clinicopathological classification Eur. Heart J., February 2, 2001; 22(4): 269 - 270. [PDF]