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Differential patterns of human cytomegalovirus gene expression in various T‐cell lines carrying human T‐cell leukemia‐lymphoma virus type I: Role of tax‐activated cellular transcription factors
Author(s) -
Beck Zoltán,
Bácsi Attila,
Liu Xiangdong,
Ebbesen Peter,
Andirkó István,
Csoma Eszter,
Kónya József,
Nagy Etelka,
Tóth Ferenc D.
Publication year - 2003
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.10447
Subject(s) - human cytomegalovirus , biology , jurkat cells , cell culture , creb , virology , transcription factor , microbiology and biotechnology , viral replication , virus , gene , t cell , immunology , genetics , immune system
Replication of human cytomegalovirus (HCMV) was investigated in various T‐cell lines expressing the tax gene product of human T‐cell leukemia‐lymphoma virus type I (HTLV‐I). Differential patterns of HCMV replication were found in HTLV‐I‐carrying cell lines. HCMV gene expression was restricted to the immediate‐early genes in MT‐2 and MT‐4 cells, whereas full replication cycle of the virus was observed in C8166‐45 cells. Productive HCMV infection induced a cytopathic effect resulting in the lysis of infected cells. The results of electrophoretic mobility shift assay (EMSA) showed high levels of NF‐κB‐, CREB/ATF‐1‐, and SRF‐specific DNA binding activity in all Tax‐positive cell lines. In contrast, SP1 activity could be detected only in C8166‐45 cells. Using an inducible system (Jurkat cell line JPX‐9), a dramatic increase in NF‐κB, CREB/ATF‐1, SRF, and SP1 binding activity, as well as productive HCMV infection, were observed upon Tax expression. Overexpression of SP1 in MT‐2 and MT‐4 cells converted HCMV infection from an abortive to a productive one. These data suggest that the stimulatory effect of Tax protein on HCMV in T cells is accomplished through at least five host‐related transcription factor pathways. The results of this study provide possible mechanisms whereby HCMV infections might imply suppression of adult T‐cell leukemia. J. Med. Virol. 71:94–104, 2003. © 2003 Wiley‐Liss, Inc.