Involvement of β2-microglobulin and integrin α(v)β3 molecules in the coxsackievirus A9 infectious cycle

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 α(v)β3 and MHC class I molecules in the coxsackievirus A9 (CAV-9) infectious cycle. Binding experiments utilizing CHO cells transfected and expressing human integrin α(v)β3, revealed that CAV-9 particles were able to bind to cells, but did not initiate a productive cell infection. Antibodies specific for integrin α(v)β3 molecules significantly reduced CAV-9 infection in susceptible cell lines. Moreover, MAbs specific for β₂-microglobulin (β₂-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 β₂-m- or integrin α(v)β3-specific antibodies. The results showed a reduction in CAV-9 binding in the presence of integrin α(v)β3-specific antibodies while there was no reduction in the presence of β₂-m-specific MAb. Taken together, these data suggest that integrin α(v)β3 is required for CAV-9 attachment but is not sufficient for cell entry, while β₂-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.