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More recent swine vesicular disease virus isolates retain binding to coxsackie–adenovirus receptor, but have lost the ability to bind human decay-accelerating factor (CD55)

Miguel A. Jimenez-Clavero^1,

¹ Department of Biotechnology, National Institute for Agriculture and Food Research and Technology, Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria (INIA), Ctra Coruña km 7·5, 28040 Madrid, Spain
² Virus Receptor and Immune Evasion Group, Department of Medical Biochemistry and Immunology, Cardiff University School of Medicine, Third Floor Henry Wellcome Research Institute, Heath Park, Cardiff CF14 4XN, UK

Correspondence
O. Brad Spiller
SpillerB{at}cardiff.ac.uk

Swine vesicular disease virus (SVDV) evolved from coxsackie B virus serotype 5 (CVB5) in the recent past, crossing the species barrier from humans to pigs. Here, SVDV isolates from early and recent outbreaks have been compared for their capacity to utilize the progenitor virus receptors coxsackie–adenovirus receptor (CAR) and decay-accelerating factor (DAF; CD55). Virus titre of CVB5 and SVDV isolates It'66 and UK'72 on human HeLa cells was reduced by pre-incubation with either anti-DAF or anti-CAR antibodies; however, recent SVDV isolates R1072, R1120 and SPA'93 did not infect HeLa cells lytically. CVB5 and SVDV infection of the pig cell line IB-RS-2 was inhibited completely by anti-CAR antibodies for all isolates, and no reduction was observed following pre-incubation of cells with anti-pig DAF antibodies. Expression of human DAF in the pig cell line IB-RS-2 enhanced the virus titre of early SVDV isolates by 25-fold, but had no effect on recent SVDV isolate titre. Binding of radiolabelled CVB5 to IB-RS-2 cells was increased seven- to eightfold by expression of human DAF and binding of early SVDV isolates was increased 1·2–1·3-fold, whereas no increase in binding by recent SVDV isolates was mediated by human DAF expression. Addition of soluble hDAF-Fc inhibited CVB5, but not SVDV, infection of pig cells. Pre-incubation of all viruses with soluble hCAR-Fc blocked infection of IB-RS-2 pig cells completely; titration of the amount of soluble hCAR-Fc required to block infection revealed that early isolate UK'72 was the least susceptible to inhibition, and the most recent isolate, SPA'93, was the most susceptible.

Present address: Departamento de Enfermedades Emergentes, Laboratorio Central de Veterinaria, Ctra Algete km 8, 28110 Algete (Madrid), Spain.

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