Receptors for Coxsackieviruses and Echoviruses

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Abstract
Studies in the late 1950s demonstrated that homogenates of particular tissues could adsorb picornaviruses, including some echoviruses and coxsackieviruses, and correlated virus adsorption with susceptibility to infection. The understanding of the receptors for group B coxsackieviruses (CVBs) is largely based on work carried out in the beginning of 1960s, and culminating in the identification of two receptor molecules within the past 5 years. Attachment-interference studies, in which saturation of cellular receptors by one virus was found to prevent attachment of a related virus, identified several picornavirus receptor families, whose members were likely to share receptors. Decay-accelerating factor (DAF) is expressed on many cell types and functions to protect cells from lysis by autologous complement. DAF is a member of a family of complement regulatory proteins composed of homologous short consensus repeat (SCR) domains. Consistent with the original observation that all six CVB serotypes compete for a single receptor, Coxsackievirus and adenovirus receptor (CAR) has been shown to mediate infection by laboratory and clinical isolates belonging to all six serotypes, including viruses like CVB3-rhabdomyosarcoma (RD) that also interact with DAF. The observation that CAR-transfected rodent cells become infected, while DAF-transfected CHO cells do not, suggests that DAF cannot perform some postattachment function essential for virus infection. Recent experiments confirm that ICAM-1 is in fact a receptor for group A coxsackieviruses (CVA)21. Infection by a variety of echovirus serotypes, as well as by CVA9, was reportedly inhibited by a monoclonal antibody to a 44-kDa cell surface protein.