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Echovirus infection of rhabdomyosarcoma cells is inhibited by antiserum to the complement control protein CD59

Division of Virology, Institute of Biomedical and Life Sciences, University of Glasgow, Church Street, Glasgow G11 5JR, UK¹
School of Animal and Microbial Science, The University of Reading, Whiteknights, PO Box 228, Reading RG6 5AJ, UK²
Complement Biology Group, Dept of Medical Biochemistry, University of Wales College of Medicine, 3rd Floor, Tenovus Building, Heath Park, Cardiff CF14 4XN, UK³

Author for correspondence: David Evans. Fax +44 141 330 6249. e-mail David.Evans{at}vir.gla.ac.uk

A number of echoviruses use decay accelerating factor (DAF) as a cellular receptor or attachment protein for cell infection. Binding of echovirus 7 to DAF at the cell surface, but not to soluble DAF in solution, triggers the formation of virus particles exhibiting an altered sedimentation coefficient (‘A’ particles) which are considered indicative of the particle uncoating process. We have previously demonstrated that antibodies to ₂-microglobulin block cell infection at a stage prior to ‘A’ particle formation and suggested that this reflects the involvement of ₂-microglobulin (or the associated MHC-I) in a virus–receptor complex that forms at the cell surface. We demonstrate here that antiserum to CD59 specifically blocks infection of rhabdomyosarcoma cells by a range of echoviruses, including viruses that bind DAF (e.g. echovirus 7) and those that use currently unidentified receptors other than DAF. The block occurs prior to ‘A’ particle formation and is cell-type specific. The potential role of CD59 as an active member, or passive participant, in the virus–receptor complex is discussed.

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