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Journal of Virology, November 1998, p. 9407-9412, Vol. 72, No. 11
Department of Microbiology, Faculty of
Medicine, The University of Newcastle, Newcastle New South Wales
2300, Australia
Received 21 May 1998/Accepted 21 July 1998
Decay-accelerating factor (DAF) mediates cellular attachment for
many human picornaviruses. In most cases, viral binding to DAF is
itself insufficient to permit cell infectivity, with a second,
functional internalization receptor being required to facilitate this
process. Previously, we postulated that the role of DAF in enterovirus
cell infection is as a sequestration receptor, maintaining a reservoir
of bound virus in an infectious state, awaiting interaction with
functional internalization receptors. Many of these functional
receptors possess the capacity to induce relatively rapid changes in
capsid conformations, resulting in the formation of altered particles
(A-type particles). In this report, we show that antibody-cross-linked
DAF, in contrast to endogenous surface-expressed forms, can act as a
functional virus receptor to mediate coxsackie A21 virus (CAV21) lytic
cell infection. In contrast to the situation with ICAM-1-mediated CAV21
infection, in which high levels of A-type particles are formed,
cross-linked DAF-induced CAV21 replication occurs in the absence of
detectable A-particle formation.
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Viral Cell Entry Induced by Cross-Linked
Decay-Accelerating Factor
*
Mailing address: Discipline of Pathology, Faculty of
Medicine, Level 3, David Madisson Clinical Sciences Building, Royal
Newcastle Hospital, Newcastle, New South Wales 2300, Australia. Phone:
61 49 23 6158. Fax: 61 49 23 6814. E-mail:
dshafren{at}mail.newcastle.edu.au.
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