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J Gen Virol. 2000 Apr;81(Pt 4):889-94.

Cytoplasmic interactions between decay-accelerating factor and intercellular adhesion molecule-1 are not required for coxsackievirus A21 cell infection.

Author information

1
Picornaviral Research Unit, Discipline of Immunology and Microbiology, Faculty of Medicine and Health Sciences, The University of Newcastle, Level 3, Royal Newcastle Hospital, Newcastle, New South Wales, Australia. dshafren@mail.newcastle.edu.au

Abstract

Coxsackievirus A21 (CAV-21) employs a cell receptor complex of decay-accelerating factor (DAF) and intercellular adhesion molecule-1 (ICAM-1) for cell infectivity. In this study, the nature of potential extra- and/or intracellular interactions between DAF and ICAM-1 involved in picornaviral cell entry was investigated. Firstly, it was shown that intracellular interplay between DAF and ICAM-1 is not required for CAV-21 infection, as CAV-21 lytic infection mediated via the DAF/ICAM-1 receptor complex is not inhibited by replacement of the transmembrane and cytoplasmic domains of ICAM-1 with those from an unrelated cell surface molecule, CD36. By immunoprecipitation, chemical cross-linking and picornaviral binding assays, the existence of a close spatial association between DAF and ICAM-1 on the surface of ICAM-1-transfected RD cells was confirmed. Furthermore, it was shown that potential extracellular DAF/ICAM-1 interactions are likely to occur in an area on or proximal to DAF SCR3 and may influence the route of CAV-21 cell entry.

PMID:
10725413
DOI:
10.1099/0022-1317-81-4-889
[Indexed for MEDLINE]

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