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Journal of Virology, December 1999, p. 10525-10530, Vol. 73, No. 12
Department of
Medicine1 and Departments of
Microbiology and Molecular Genetics,2 Harvard
Medical School, Channing Laboratory, Brigham and Women's Hospital,
Boston, Massachusetts 02115
Received 24 May 1999/Accepted 2 September 1999
An Epstein-Barr virus (EBV) recombinant (MS231) that expresses the
first 231 amino acids (aa) of LMP1 and is truncated 155 aa before the
carboxyl terminus transformed resting B lymphocytes into lymphoblastoid
cell lines (LCLs) only when the infected cells were grown on fibroblast
feeder cells (K. M. Kaye et al., J. Virol. 69:675-683,
1995). Higher-titer MS231 virus has now been compared to wild-type (WT)
EBV recombinants for the ability to cause resting primary B-lymphocyte
transformation. Unexpectedly, MS231 is as potent as WT EBV recombinants
in causing infected B lymphocytes to proliferate in culture for up to 5 weeks. When more than one transforming event is initiated in a
microwell, the MS231 recombinant supports efficient long-term LCL
outgrowth and fibroblast feeder cells are not required. However, with
limited virus input, MS231-infected cells differed in their growth from
WT virus-infected cells as early as 6 weeks after infection. In
contrast to WT virus-infected cells, most MS231-infected cells could
not be grown into long-term LCLs. Thus, the LMP1 amino-terminal 231 aa
are sufficient for initial growth transformation but the
carboxyl-terminal 155 aa are necessary for efficient long-term
outgrowth. Despite the absence of the carboxyl-terminal 155 aa, MS231-
and WT-transformed LCLs are similar in latent EBV gene expression, in
ICAM-1 and CD23 expression, and in NF-
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
An Epstein-Barr Virus That Expresses Only the First
231 LMP1 Amino Acids Efficiently Initiates Primary B-Lymphocyte
Growth Transformation

and
B and c-jun N-terminal kinase
activation. MS231 recombinant-infected LCLs, however, require 16- to
64-fold higher cell density than WT-infected LCLs for regrowth after
limiting dilution. These data indicate that the LMP1 carboxyl-terminal 155 aa are important for growth at lower cell density and appear to
reduce dependence on paracrine growth factors.
*
Corresponding author. Mailing address: Channing
Laboratory, Brigham and Women's Hospital, 181 Longwood Ave., Boston,
MA 02115. Phone: (617) 525-4256. Fax: (617) 525-4251. E-mail:
kkaye{at}rics.bwh.harvard.edu.
Present address: GelTex Pharmaceuticals, Inc., Waltham, MA 02154.
Present address: Department of Microbiology and Immunology,
Northwestern University, Chicago, Ill.
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