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Journal of Virology, February 2003, p. 2207-2213, Vol. 77, No. 3
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.3.2207-2213.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

The Promyelocytic Leukemia Protein Does Not Mediate Foamy Virus Latency In Vitro

Christopher D. Meiering and Maxine L. Linial^*

Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, and Department of Microbiology, University of Washington, Seattle, Washington 98195

Received 20 August 2002/ Accepted 5 November 2002

Spumaviruses, commonly called foamy viruses, are complex retroviruses that establish life-long persistent infections in the absence of accompanying pathology. Depending upon cell type, infection of cells in tissue culture cells can result in either lytic replication, persistence, or latency. The cellular factors that mediate foamy virus (FV) latency are poorly understood. In this study we show that the only known inhibitor of FV replication, the promyelocytic leukemia protein (PML), which binds the FV transactivator (Tas), does not play an important role in FV latency in vitro. We found no significant differences in PML levels in cells that supported lytic replication compared to those that were latently infected. Furthermore, endogenous PML levels did not change following exposure to phorbol myristate acetate (PMA), which induces FV replication. We demonstrated that FV replication proceeded in the presence of substantial levels of PML, both in fully permissive cells and during reactivation of latent FV. Endogenous PML did not efficiently colocalize with Tas, even after upregulation by alpha interferon (IFN-) treatment. IFN- did, however, partially suppress the reactivation of latent FV by PMA. Finally, depletion of endogenous PML by small interfering RNA did not promote activation of FV in cells that responded to PMA treatment. Taken together, these data indicate that endogenous PML does not play an important role in mediating FV latency.

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* Corresponding author. Mailing address: Division of Basic Sciences, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., Seattle, WA 98109. Phone: (206) 667-4442. Fax: (206) 667-5939. E-mail: mlinial{at}fhcrc.org.

Present address: Department of Microbiology & Immunology, Stanford School of Medicine, Stanford, CA 94305.

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Journal of Virology, February 2003, p. 2207-2213, Vol. 77, No. 3
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.3.2207-2213.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

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