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Animal: RNA Viruses |
vß3 molecules in the coxsackievirus A9 infectious cycle
Department of Biological Sciences, Central Campus, University of Essex, Wivenhoe Park, Colchester CO4 3SQ, UK1
Department of Vascular Biology, The Scripps Research Institute, La Jolla, California 92037, USA2
Author for correspondence: Martha Triantafilou.Fax +44 1206 872592. e-mail mtrian{at}essex.ac.uk
It is becoming apparent that many viruses employ more than one cell surface molecule for their attachment and cell entry. In this study, we have tested the role of integrin
vß3 and MHC class I molecules in the coxsackievirus A9 (CAV-9) infectious cycle. Binding experiments utilizing CHO cells transfected and expressing human integrin
vß3, revealed that CAV- 9 particles were able to bind to cells, but did not initiate a productive cell infection. Antibodies specific for integrin
vß3 molecules significantly reduced CAV-9 infection in susceptible cell lines. Moreover, MAbs specific for ß2- microglobulin (ß2-m) and MHC class I molecules completely inhibited CAV-9 infection. To assess the effect of these antibodies on virus binding, we analysed CAV-9 binding by flow cytometry in the presence of ß2-m- or integrin
vß3-specific antibodies. The results showed a reduction in CAV-9 binding in the presence of integrin
vß3- specific antibodies while there was no reduction in the presence of ß2-m-specific MAb. Taken together, these data suggest that integrin
vß3 is required for CAV-9 attachment but is not sufficient for cell entry, while ß2 -m, although not directly involved in CAV-9 binding, plays a post- attachment role in the CAV-9 infectious process, possibly being involved in virus entry.
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