Virally induced changes in cellular microRNAs maintain latency of human cytomegalovirus in CD34+ progenitors

One site of latency of human cytomegalovirus (HCMV; human herpesvirus 5) is known to be CD34(+) haematopoietic progenitor cells, and it is likely that carriage of latent virus has profound effects on cellular gene expression in order to optimize latency and reactivation. As microRNAs (miRNAs) play i...

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Bibliographic Details
Published in:Journal of general virology 2011-07, Vol.92 (Pt 7), p.1539-1549
Main Authors: POOLE, Emma, MCGREGOR DALLAS, Stuart R, COLSTON, Julia, JOSEPH, Robert Samuel V, SINCLAIR, John
Format: Article
Language:English
Subjects:
Antigens, CD34 - genetics
Antigens, CD34 - metabolism
Biological and medical sciences
Cell Line
Cytomegalovirus - genetics
Cytomegalovirus - physiology
Cytomegalovirus Infections - genetics
Cytomegalovirus Infections - metabolism
Cytomegalovirus Infections - virology
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation
Hematopoietic Stem Cells - metabolism
Hematopoietic Stem Cells - virology
Humans
Microbiology
MicroRNAs - genetics
MicroRNAs - metabolism
Miscellaneous
Virology
Virus Latency
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Summary:One site of latency of human cytomegalovirus (HCMV; human herpesvirus 5) is known to be CD34(+) haematopoietic progenitor cells, and it is likely that carriage of latent virus has profound effects on cellular gene expression in order to optimize latency and reactivation. As microRNAs (miRNAs) play important roles in regulating stem-cell gene expression, this study asked whether latent carriage of HCMV led to changes in cellular miRNA expression. A comprehensive miRNA screen showed the differential regulation of a number of cellular miRNAs during HCMV latency in CD34(+) progenitor cells. One of these, hsa-miR-92a, was robustly decreased in three independent miRNA screens. Latency-induced change in hsa-miR-92a results in an increase in expression of GATA-2 and subsequent increased expression of cellular IL-10, which aids the maintenance of latent viral genomes in CD34(+) cells, probably resulting from their increased survival.
ISSN:0022-1317
1465-2099
DOI:10.1099/vir.0.031377-0