This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Huber, S A Articles by Schwimmbeck, P Search for Related Content PubMed PubMed Citation Articles by Huber, S A Articles by Schwimmbeck, P

 Previous Article  |  Next Article 

J Virol. 1994 January; 68(1): 195-206

Augmentation of pathogenesis of coxsackievirus B3 infections in mice by exogenous administration of interleukin-1 and interleukin-2.

Department of Pathology, University of Vermont, Burlington 05405.

ABSTRACT

Two variants of coxsackievirus B3 (CVB3) which differ dramatically in the ability to induce myocarditis in BALB/c mice were studied. H3 virus infection of murine monocytes in vitro resulted in release of concentrations of interleukin 1 (IL-1) and alpha/beta interferon that were high compared with those of cells infected with the H310A1 virus variant. In vivo, H3 virus infection caused substantial inflammatory cell infiltration of the myocardium, and lymphocytes from these animals gave predominantly Th1-cell responses to either whole H3 virus or overlapping peptides of the CVB3 vp1 capsid protein, as determined by IL-2 production. In contrast, H310A1 virus infection produced minimal myocarditis and Th1-cell responses, but Th2-cell activation was more pronounced than in H3 virus-infected mice (as determined by IL-4 concentrations). Exogenous treatment of H310A1 virus-infected mice with either IL-1 or IL-2 restored both myocarditis susceptibility and Th1-cell responses to whole virus and vp1 peptides. Furthermore, H310A1 virus-infected mice given exogenous IL-1 showed substantial in situ IL-2 deposition in the myocardium. These results indicate that CVB3-induced myocarditis may depend upon release of specific cytokines during infection and that activation of Th1 cells may be an important factor in pathogenesis.

This article has been cited by other articles:

• Smith, A. D., Botero, S., Levander, O. A. (2008). Copper Deficiency Increases the Virulence of Amyocarditic and Myocarditic Strains of Coxsackievirus B3 in Mice. J. Nutr. 138: 849-855 [Abstract] [Full Text]  
• Fairweather, D., Yusung, S., Frisancho, S., Barrett, M., Gatewood, S., Steele, R., Rose, N. R. (2003). IL-12 Receptor {beta}1 and Toll-Like Receptor 4 Increase IL-1{beta}- and IL-18-Associated Myocarditis and Coxsackievirus Replication. J. Immunol. 170: 4731-4737 [Abstract] [Full Text]  
• Huber, S., Sartini, D., Exley, M. (2003). Role of CD1d in Coxsackievirus B3-Induced Myocarditis. J. Immunol. 170: 3147-3153 [Abstract] [Full Text]  
• Liu, P., Lee, P., Fuse, K., Nian, M. (2002). Molecular pathophysiological mechanisms in virus infected host myocardium. Eur Heart J Suppl 4: I37-I41 [Abstract]  
• Li, J., Lothar Schwimmbeck, P., Tschope, C., Leschka, S., Husmann, L., Rutschow, S., Reichenbach, F., Noutsias, M., Kobalz, U., Poller, W., Spillmann, F., Zeichhardt, H., Schultheiss, H.-P., Pauschinger, M. (2002). Collagen degradation in a murine myocarditis model: relevance of matrix metalloproteinase in association with inflammatory induction. Cardiovasc Res 56: 235-247 [Abstract] [Full Text]  
• Huber, S. A., Sartini, D., Exley, M. (2002). V{gamma}4+ T Cells Promote Autoimmune CD8+ Cytolytic T-Lymphocyte Activation in Coxsackievirus B3-Induced Myocarditis in Mice: Role for CD4+ Th1 Cells. J. Virol. 76: 10785-10790 [Abstract] [Full Text]  
• Huber, S., Shi, C., Budd, R. C. (2002). {gamma}{delta} T Cells Promote a Th1 Response during Coxsackievirus B3 Infection In Vivo: Role of Fas and Fas Ligand. J. Virol. 76: 6487-6494 [Abstract] [Full Text]  
• Henke, A., Zell, R., Ehrlich, G., Stelzner, A. (2001). Expression of Immunoregulatory Cytokines by Recombinant Coxsackievirus B3 Variants Confers Protection against Virus-Caused Myocarditis. J. Virol. 75: 8187-8194 [Abstract] [Full Text]  
• Huber, S. A., Graveline, D., Newell, M. K., Born, W. K., O'Brien, R. L. (2000). V{gamma}1+ T Cells Suppress and V{gamma}4+ T Cells Promote Susceptibility to Coxsackievirus B3-Induced Myocarditis in Mice. J. Immunol. 165: 4174-4181 [Abstract] [Full Text]  
• Nishio, R., Matsumori, A., Shioi, T., Ishida, H., Sasayama, S. (1999). Treatment of Experimental Viral Myocarditis With Interleukin-10. Circulation 100: 1102-1108 [Abstract] [Full Text]  
• Huber, S. A., Kupperman, J., Newell, M. K. (1999). Hormonal Regulation of CD4+ T-Cell Responses in Coxsackievirus B3-Induced Myocarditis in Mice. J. Virol. 73: 4689-4695 [Abstract] [Full Text]  
• Kawai, C. (1999). From Myocarditis to Cardiomyopathy: Mechanisms of Inflammation and Cell Death : Learning From the Past for the Future. Circulation 99: 1091-1100 [Abstract] [Full Text]  
• Nakamura, H., Yamamura, T., Umemoto, S., Fukuta, S., Shioi, T., Matsumori, A., Sasayama, S., Matsuzaki, M. (1996). Autoimmune Response in Chronic Ongoing Myocarditis Demonstrated by Heterotopic Cardiac Transplantation in Mice. Circulation 94: 3348-3354 [Abstract] [Full Text]  
• Kanda, T., Wilson McManus, J. E., Nagai, R., Imai, S., Suzuki, T., Yang, D., McManus, B. M., Kobayashi, I. (1996). Modification of Viral Myocarditis in Mice by Interleukin-6. Circ. Res. 78: 848-856 [Abstract] [Full Text]