MODEL OF EPSTEIN-BARR-VIRUS INFECTION OF HUMAN THYMOCYTES - EXPRESSION OF VIRAL GENOME AND IMPACT ON CELLULAR RECEPTOR EXPRESSION IN THE LYMPHOBLASTIC CELL-LINE, HPB-ALL
Rlk. Paterson et al., MODEL OF EPSTEIN-BARR-VIRUS INFECTION OF HUMAN THYMOCYTES - EXPRESSION OF VIRAL GENOME AND IMPACT ON CELLULAR RECEPTOR EXPRESSION IN THE LYMPHOBLASTIC CELL-LINE, HPB-ALL, Blood, 85(2), 1995, pp. 456-464
Infection of B lymphocytes and epithelial tissue by Epstein-Barr virus
(EBV) is associated with malignancy and autoimmunity. The cellular re
ceptor for EBV has been identified as CD21 (CR2). A molecule, which is
biochemically and immunologically similar to B-cell CD21, has been id
entified 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 tu
mors of T-cell origin. We have evaluated the susceptibility of the hum
an immature T cell line, HPB-ALL, to infection by EBV. Electron micros
copy studies showed a rapid internalization of virus by HPB cells. Sou
thern blotting showed the intracellular presence of linear EBV genomes
, and components of the virus replicative cycle were identified. Expre
ssion of the BamHI Z region of the genome, encoding the nuclear protei
n, 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 obs
erved to occur transiently. Infection of HPB cells was also accompanie
d by altered expression of T-cell surface molecules involved in antige
n 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. (C) 1995 by The American Society of Hematol
ogy.