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Journal of Virology, September 1999, p. 7722-7733, Vol. 73, No. 9
INSERM U519, 76000 Rouen,
France1; Institut für Medizinische
Mikrobiologie und Hygiene, Universität Regensburg, D-93053
Regensburg, Germany3; and Institut
für Hygiene2 and Institut
für Allgemeine und Experimentelle
Pathologie,4 Universität Innsbruck, A-6020
Innsbruck, Austria
Received 19 January 1999/Accepted 21 May 1999
Epstein-Barr virus (EBV) is implicated in different central nervous
system syndromes. The major cellular receptor for EBV, complement
receptor type 2 (CR2) (CD21), is expressed by different astrocyte cell
lines and human fetal astrocytes, suggesting their susceptibility to
EBV infection. We demonstrated the infection of two astrocyte cell
lines, T98 and CB193, at low levels. As infection was mediated by CR2,
we used two stable CR2 transfectant astrocyte cell lines (T98CR2 and
CB193CR2) to achieve a more efficient infection. We have monitored EBV
gene expression for 2 months and observed the transient infection of
T98 and T98CR2 cells and persistent infection of CB193 and CB193CR2
cells. The detection of BZLF1, BALF2, and BcLF1 mRNA expression
suggests that the lytic cycle is initiated at early time points
postinfection. At later time points the pattern of mRNA expressed
(EBER1, EBNA1, EBNA2, and LMP1) differs from latency type III in the
absence of LMP2A transcription and in the expression of BALF2 and BcLF1
but not BZLF1. A reactivation of the lytic cycle was achieved in
CB193CR2 cells by the addition of phorbol esters. These studies
identify astrocyte cell lines as targets for EBV infection and suggest that this infection might play a role in the pathology of EBV in the brain.
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Epstein-Barr Virus Infection of Human Astrocyte
Cell Lines
*
Corresponding author. Present address: INSERM U519,
Faculté de Médecine et de Pharmacie, 38 Blvd.
Gambetta, 76000 Rouen, France. Phone: 33-2-35-14-85-42. Fax:
33-2-35-14-85-41. E-mail: annemenet{at}hotmail.com.
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