Resumen
BK polyomavirus causes disease in immunosuppressed patients. BK virus replication was augmented in HEL-299 cells cultured in conditions that activated the MAP kinase, ERK1/2. To determine if MAP kinase activation increased BK virus replication, cells were treated with serum and phorbol 12-myristate 13-acetate (PMA). Serum and PMA stimulated large T-antigen expression and increased BK virus DNA replication. The effects of serum/PMA were directly related to MAP kinase signal activation since viral replication was reduced by the MEK1/2 inhibitor U0126. PMA also increased cyclin D1 expression and inhibition of cyclin D1/CDK4 complex and the cell cycle reduced BK virus infection. The PMA effect occurred independent of direct transcriptional activation of the viral NCCR. In HEL-299 cells, virus infection in high serum and PMA accelerated viral replication that resulted, within 7 days, in the production of high titer infectious BK virus. These results show that MAP kinase signal activation increases BK virus replication.
Idioma original | English |
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Páginas (desde-hasta) | 21-29 |
Número de páginas | 9 |
Publicación | Journal of Virological Methods |
Volumen | 170 |
N.º | 1-2 |
DOI | |
Estado | Published - dic. 2010 |
Nota bibliográfica
Funding Information:Supported by operating grants from the Canadian Institutes for Health Research and infrastructure grants from the Canadian Foundation for Innovation . D.A.M. holds a Tier II Canada Research Chair. D.A.M. and P.L.B are recipients of Alberta Heritage Foundation for Medical Research Clinical Senior Scholar Awards.
ASJC Scopus Subject Areas
- Virology
PubMed: MeSH publication types
- Journal Article
- Research Support, Non-U.S. Gov't