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Journal of Virology, May 2000, p. 4284-4290, Vol. 74, No. 9
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.
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
*
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.
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