Comparative analysis of two coxsackievirus B3 strains: Putative influence of virus-receptor interactions on pathogenesis
Corresponding Author
Dr. H.-C. Selinka
Department of Molecular Pathology, University Hospital Tübingen, Tübingen, Germany
Institute for Medical Microbiology and Hygiene, University of Mainz, Mainz, Germany
Institute of Medical Microbiology and Hygiene, University of Mainz, Obere Zahlbacherstr. 67, D-55101 Mainz, Germany.===Search for more papers by this authorA. Wolde
Department of Molecular Pathology, University Hospital Tübingen, Tübingen, Germany
Search for more papers by this authorA. Pasch
Department of Molecular Pathology, University Hospital Tübingen, Tübingen, Germany
Search for more papers by this authorK. Klingel
Department of Molecular Pathology, University Hospital Tübingen, Tübingen, Germany
Search for more papers by this authorJ.-J. Schnorr
Department of Molecular Pathology, University Hospital Tübingen, Tübingen, Germany
Search for more papers by this authorJ.-H. Küpper
Department of Molecular Pathology, University Hospital Tübingen, Tübingen, Germany
Search for more papers by this authorA.M. Lindberg
Department of Chemistry and Biomedical Sciences, University of Kalmar, Kalmar, Sweden
Search for more papers by this authorR. Kandolf
Department of Molecular Pathology, University Hospital Tübingen, Tübingen, Germany
Search for more papers by this authorCorresponding Author
Dr. H.-C. Selinka
Department of Molecular Pathology, University Hospital Tübingen, Tübingen, Germany
Institute for Medical Microbiology and Hygiene, University of Mainz, Mainz, Germany
Institute of Medical Microbiology and Hygiene, University of Mainz, Obere Zahlbacherstr. 67, D-55101 Mainz, Germany.===Search for more papers by this authorA. Wolde
Department of Molecular Pathology, University Hospital Tübingen, Tübingen, Germany
Search for more papers by this authorA. Pasch
Department of Molecular Pathology, University Hospital Tübingen, Tübingen, Germany
Search for more papers by this authorK. Klingel
Department of Molecular Pathology, University Hospital Tübingen, Tübingen, Germany
Search for more papers by this authorJ.-J. Schnorr
Department of Molecular Pathology, University Hospital Tübingen, Tübingen, Germany
Search for more papers by this authorJ.-H. Küpper
Department of Molecular Pathology, University Hospital Tübingen, Tübingen, Germany
Search for more papers by this authorA.M. Lindberg
Department of Chemistry and Biomedical Sciences, University of Kalmar, Kalmar, Sweden
Search for more papers by this authorR. Kandolf
Department of Molecular Pathology, University Hospital Tübingen, Tübingen, Germany
Search for more papers by this authorAbstract
Strain-specific differences in the interaction of coxsackievirus B3 (CVB3) with the coxsackievirus-adenovirus receptor (CAR) and the decay-accelerating factor (DAF) co-receptor proteins were investigated using a non-haemagglutinating (CVB3) and a haemagglutinating (CVB3-HA) strain of CVB3. A panel of receptor-transfected hamster CHO cells, expressing either CAR (CHOCAR cells), DAF (CHODAF cells), or both receptor proteins (CHODC cells) were used to study the interplay of CAR and DAF receptor molecules with regard to binding and infection with CVB3 and CVB3-HA. Despite clear differences in their binding phenotypes, both virus strains were found to primarily depend on the CAR receptor protein for initialization of productive infections. Cytopathic effects induced by CVB3-HA were influenced by co-expression of DAF receptor proteins. The cardiotropic potential of both virus strains was investigated in A.BY/SnJ mice. Despite comparable virus replication of both CVB3 strains in individual myocytes, the number of infected heart muscle cells was significantly lower in CVB3-HA infected mice. Infections of pancreata correlated with myocardial infections. Together these data suggest that even small differences in virus-receptor interactions, influencing virus binding and virus spread, may have an impact on the pathogenesis of CVB-induced diseases. J. Med. Virol. 67:224–233, 2002. © 2002 Wiley-Liss, Inc.
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