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Model of Epstein-Barr virus infection of human thymocytes: expression of
viral genome and impact on cellular receptor expression in the T-
lymphoblastic cell line, HPB-ALL
RL Paterson, C Kelleher, TD Amankonah, JE Streib, JW Xu, JF Jones and EW Gelfand
Department of Pediatrics, National Jewish Center for Immunology and
Respiratory Medicine, Denver, CO 80206.
Infection of B lymphocytes and epithelial tissue by Epstein-Barr virus
(EBV) is associated with malignancy and autoimmunity. The cellular receptor
for EBV has been identified as CD21 (CR2). A molecule, which is
biochemically and immunologically similar to B-cell CD21, has been
identified on a subpopulation of immature thymocytes, suggesting a role for
this molecule in the regulation of T-cell development and further
suggesting that immature T cells might be susceptible to EBV infection. A
growing body of literature now documents the presence of EBV in tumors of
T-cell origin. We have evaluated the susceptibility of the human immature T
cell line, HPB-ALL, to infection by EBV. Electron microscopy studies showed
a rapid internalization of virus by HPB cells. Southern blotting showed the
intracellular presence of linear EBV genomes, and components of the virus
replicative cycle were identified. Expression of the BamHI Z region of the
genome, encoding the nuclear protein, ZEBRA, which is strictly associated
with productive infection in B cells, was detected in HPB-ALL cells. A
spliced variant of Z, RAZ, was also identified. Cell surface expression of
EBV late antigens was observed to occur transiently. Infection of HPB cells
was also accompanied by altered expression of T-cell surface molecules
involved in antigen recognition, a process critical to normal development
of the T-cell repertoire. Delineation of the outcome of T- cell infection
by EBV may lead to a better understanding of the role of this virus in
autoimmune processes and malignancy.
Volume 85,
Issue 2,
pp. 456-464,
01/15/1995
Copyright © 1995 by The American Society of Hematology
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