Growth of coxsackievirus B3 in RD cells selects for a virus strain that utilizes decay-accelerating factor (DAF/CD55) for cell surface attachment.
DAF may mediate adapted CB3 entry; leaves open receptor-targeted strategies in human myocarditis.
A coxsackievirus B3 (CB3) isolate adapted to growth in RD cells shows an alteration in cell tropism as a result of its capacity to bind a 70-kDa cell surface molecule expressed on these cells. We now show that this molecule is the complement regulatory protein, decay-accelerating factor (DAF) (CD55). Anti-DAF antibodies prevented CB3 attachment to the cell surface. Radiolabeled CB3 adapted to growth in RD cells bound to CHO cells transfected with human DAF, whereas CB3 (strain Nancy), the parental strain, did not bind to DAF transfectants. These results indicate that growth of CB3 in RD cells selected for a virus strain that uses DAF for cell surface attachment.
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Bergelson et al. (1995) studied this question.
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