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Journal of Virology, November 2000, p. 10142-10152, Vol. 74, No. 21
Department of Gene
Vectors1 and Clinical Cooperation Group,
Gene Therapy of Hematopoietic Neoplasia,3
GSF-National Research Center for Environment and Health, 81377 Munich,
and Robert-Koch Institute, 13353 Berlin,2 Germany
Received 14 March 2000/Accepted 11 August 2000
The binding of the viral major glycoprotein BLLF1 (gp350/220) to
the CD21 cellular receptor is thought to play an essential role during
infection of B lymphocytes by the Epstein-Barr virus (EBV). However,
since CD21-negative cells have been reported to be infectible with EBV,
additional interactions between viral and cellular molecules seem to be
probable. Based on a recombinant genomic EBV plasmid, we deleted the
gene that encodes the viral glycoprotein BLLF1. We tested the ability
of the viral mutant to infect different lymphoid and epithelial cell
lines. Primary human B cells, lymphoid cell lines, and nearly all of
the epithelial cell lines that are susceptible to wild-type EBV
infection could also be successfully infected with the viral mutant in
vitro, although the efficiency of infection with BLLF1-negative virus was clearly lower than the one observed with wild-type EBV. Our studies
show that the interaction between BLLF1 and CD21 is not absolutely
required for the infection of lymphocytes and epithelial cells,
indicating that viral molecules other than BLLF1 can mediate the
binding of EBV to its target cells. In this context, our results further suggest the hypothesis that additional cellular molecules, apart from CD21, allow virus entry into these cells.
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Infectious Epstein-Barr Virus Lacking Major
Glycoprotein BLLF1 (gp350/220) Demonstrates the Existence of Additional
Viral Ligands
*
Corresponding author. Mailing address: GSF-Institute of
Clinical Molecular Biology and Tumor Genetics, Marchioninistr. 25, 81377 Munich, Germany. Phone: 49-89-7099513. Fax: 49-89-7099500. E-mail: Delecluse{at}gsf.de.
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