Echoviruses and Coxsackie B viruses specifically bind to human DAF but not to its rodent analogues, highlighting species-specific receptor interactions.
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Rodent models may not capture EV/CBV–DAF interactions; leaves open relevance to human tropism and pathogenesis.
Many serotypes of echovirus (EV) and Coxsackie B virus (CBV) bind human decay-accelerating factor (DAF) and use it as a receptor for infection. Analogues for DAF have been isolated from mice and rats and characterized; these analogues have amino acid identities to human DAF of approximately 60%. EV serotypes 3, 6', 7, 11-13, and 29 and CBV serotypes 1, 3, and 5 caused hemagglutination of human erythrocytes but not rat or mouse erythrocytes, suggesting failure to bind rodent DAF. To confirm this evidence, radiolabeled viruses were incubated with transfected Chinese hamster ovary (CHO) cells that were abundantly expressing each type of DAF. Only cells that expressed human DAF bound virus. Although binding of EV and CBV was specific for human DAF, complement inhibition by DAF expressed in CHO cells was similar for each analogue.
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Spiller et al. (2000) studied this question.
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