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Journal of Virology, May 2000, p. 4284-4290, Vol. 74, No. 9
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Apoptosis in Coxsackievirus B3-Caused Diseases: Interaction between the Capsid Protein VP2 and the Proapoptotic Protein Siva

Andreas Henke,1,* Heike Launhardt,2 Katrin Klement,1 Axel Stelzner,1 Roland Zell,1 and Thomas Munder2

Institute of Virology, Medical Center, Friedrich Schiller University Jena,1 and Department of Cell and Molecular Biology, Hans-Knöll-Institut für Naturstoff-Forschung e.V., D-07745 Jena,2 Germany

Received 8 November 1999/Accepted 28 January 2000

Coxsackievirus B3 (CVB3) is a common factor in human myocarditis. Apoptotic events are present in CVB3-induced disease, but it is unclear how CVB3 is involved in apoptosis and which viral proteins may induce the apoptotic pathway. In this report we demonstrate that the human and murine proapoptotic protein Siva specifically interact with the CVB3 capsid protein VP2. Furthermore, the transcription of Siva is strongly induced in tissue of CVB3-infected mice and is present in the same area which is positively stained for apoptosis, CD27, and CD70. It has been proposed that Siva is involved in the CD27/CD70-transduced apoptosis. Therefore, we suggest a molecular mechanism through which apoptotic events contributes to CVB3-caused pathogenesis.


* Corresponding author. Mailing address: Institute of Virology, Medical Center, Friedrich Schiller University, Winzerlaer Str. 10, D-07745 Jena, Germany. Phone: (49) 3641 657215. Fax: (49) 3641 657202. E-mail: i6hean{at}rz.uni-jena.de.


Journal of Virology, May 2000, p. 4284-4290, Vol. 74, No. 9
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.



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