适应在RD细胞中生长的柯萨奇病毒B3与衰变加速因子（CD55）结合。
Coxsackievirus B3 adapted to growth in RD cells binds to decay-accelerating factor (CD55).
作者信息
Bergelson J M, Mohanty J G, Crowell R L, St John N F, Lublin D M, Finberg R W
机构信息
Laboratory of Infectious Diseases, Dana-Farber Cancer Institute, Boston, Massachusetts 02115.
出版信息
J Virol. 1995 Mar;69(3):1903-6. doi: 10.1128/JVI.69.3.1903-1906.1995.
Abstract
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.
摘要
一株适应在RD细胞中生长的柯萨奇病毒B3（CB3）由于其能够结合这些细胞上表达的一种70 kDa细胞表面分子，从而导致细胞嗜性发生改变。我们现在表明，该分子是补体调节蛋白衰变加速因子（DAF）（CD55）。抗DAF抗体可阻止CB3附着于细胞表面。适应在RD细胞中生长的放射性标记CB3可与转染了人DAF的CHO细胞结合，而亲代菌株CB3（Nancy株）则不与DAF转染细胞结合。这些结果表明，在RD细胞中生长的CB3选择了一种利用DAF进行细胞表面附着的病毒株。
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