The human polyomavirus BK T antigen induces gene expression in human cytomegalovirus

Co-infections or co-habitations of cells by two or more viruses may occur in the human organism. Human cytomegalovirus (HCMV) and the human polyomavirus BK (BKV) have common host cells and may both establish lifelong latency/persistence following primary infection. Both viruses may become reactivate...

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Bibliographic Details
Published in:Virus research 1997-11, Vol.52 (1), p.61-71
Main Authors: Kristoffersen, Anne K, Johnsen, John Inge, Seternes, Ole Morten, Rollag, Halvor, Degré, Miklos, Traavik, Terje
Format: Article
Language:English
Subjects:
Antigens, Viral, Tumor - physiology
BK Virus - immunology
BKV
BKV large T antigen
Cells, Cultured
Co-infection
Cytomegalovirus - genetics
Cytomegalovirus Infections - genetics
Cytomegalovirus Infections - virology
Enhancer Elements, Genetic
Gene Expression Regulation, Viral
Genes, Immediate-Early
HCMV
Humans
Promoter Regions, Genetic
Transcriptional Activation
Transfection
Tumor Cells, Cultured
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Summary:Co-infections or co-habitations of cells by two or more viruses may occur in the human organism. Human cytomegalovirus (HCMV) and the human polyomavirus BK (BKV) have common host cells and may both establish lifelong latency/persistence following primary infection. Both viruses may become reactivated by immunosuppression or other conditions which upset host–virus balance, and they encode gene products with the inherent potential of acting as heterologous transacting factors for expression of cellular or viral genes. It has been shown that HCMV induces gene expression and replication of primate polyomaviruses. We now demonstrate that BKV is able to enhance the expression of HCMV immediate early (IE1 and 2) as well as the early (E) protein pp65 during double infections in semi-permissive cells. By transfection experiments it was established that the phenomenon is due to heterologous transcriptional transactivation of the HCMV major IE promoter (MIEP) by the BKV large T antigen, without contribution from the small t antigen.
ISSN:0168-1702
1872-7492
DOI:10.1016/S0168-1702(97)00100-7