MAP kinase activation increases BK polyomavirus replication and facilitates viral propagation in vitro

Mark E. Seamone; Wenjie Wang; Philip Acott; Paul L. Beck; Lee Anne Tibbles; Daniel A. Muruve

doi:10.1016/j.jviromet.2010.08.014

MAP kinase activation increases BK polyomavirus replication and facilitates viral propagation in vitro

Mark E. Seamone, Wenjie Wang, Philip Acott, Paul L. Beck, Lee Anne Tibbles, Daniel A. Muruve

Medicine

Medicine

Research output: Contribution to journal › Article › peer-review

14 Citations (Scopus)

Abstract

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.

Original language	English
Pages (from-to)	21-29
Number of pages	9
Journal	Journal of Virological Methods
Volume	170
Issue number	1-2
DOIs	https://doi.org/10.1016/j.jviromet.2010.08.014
Publication status	Published - Dec 2010

Bibliographical note

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

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10.1016/j.jviromet.2010.08.014

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title = "MAP kinase activation increases BK polyomavirus replication and facilitates viral propagation in vitro",

abstract = "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.",

author = "Seamone, {Mark E.} and Wenjie Wang and Philip Acott and Beck, {Paul L.} and Tibbles, {Lee Anne} and Muruve, {Daniel A.}",

note = "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.",

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AU - Beck, Paul L.

AU - Tibbles, Lee Anne

AU - Muruve, Daniel A.

N1 - 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.

PY - 2010/12

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N2 - 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.

AB - 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.

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MAP kinase activation increases BK polyomavirus replication and facilitates viral propagation in vitro

Abstract

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