Repression of human cytomegalovirus major immediate early gene expression in a monocytic cell line

Department of Medicine, University of Cambridge, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, U.K. We have previously shown that a major site of persistence of human cytomegalovirus (HCMV) in healthy carriers is in peripheral blood monocytes. However, monocytes are difficult to infect...

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Bibliographic Details
Published in:Journal of general virology 1992-02, Vol.73 (2), p.433-435
Main Authors: Sinclair, J. H, Baillie, J, Bryant, L. A, Taylor-Wiedeman, J. A, Sissons, J. G. P
Format: Article
Language:English
Subjects:
Antigens, Viral - genetics
Biological and medical sciences
Cell Differentiation
Cell Line
Cytomegalovirus - genetics
Enhancer Elements, Genetic
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation, Viral
Humans
Immediate-Early Proteins
Macrophages - microbiology
Microbiology
Monocytes - microbiology
Promoter Regions, Genetic
Replicative cycle, interference, host-virus relations, pathogenicity, miscellaneous strains
Virology
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Summary:Department of Medicine, University of Cambridge, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, U.K. We have previously shown that a major site of persistence of human cytomegalovirus (HCMV) in healthy carriers is in peripheral blood monocytes. However, monocytes are difficult to infect in vitro with HCMV, and HCMV gene expression cannot be reproducibly detected in peripheral blood cells of healthy carriers. Here we show that the monocytic cell line THP1 is non-permissive for HCMV infection due to a block in expression of the HCMV major immediate early (IE) promoter. This repression is correlated with the presence of a differentiation-specific cellular factor which binds to the imperfect dyad symmetry and the 21 bp enhancer repeats of the major IE promoter regulatory region and which has characteristics of MBF1, a factor which we have previously defined in HCMV non-permissive, undifferentiated teratocarcinoma cells. Both differentiation of THP1 cells into macrophages, which results in a decrease in this factor, or deletion of the factor's binding sites from the IE promoter/enhancer lifts this repression and permits expression from the major IE promoter. Received 22 July 1991; accepted 11 October 1991.
ISSN:0022-1317
1465-2099
DOI:10.1099/0022-1317-73-2-433