This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Meiering, C. D.
Right arrow Articles by Linial, M. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Meiering, C. D.
Right arrow Articles by Linial, M. L.

 Previous Article  |  Next Article 

Journal of Virology, July 2001, p. 6547-6557, Vol. 75, No. 14
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.14.6547-6557.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Cell-Type-Specific Regulation of the Two Foamy Virus Promoters

Christopher D. Meiering,1,2 Claudia Rubio,1 Cynthia May,1 and Maxine L. Linial1,2,*

Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109,1 and Department of Microbiology, University of Washington, Seattle, Washington 981952

Received 5 February 2001/Accepted 13 April 2001

The foamy virus (FV) genome contains two promoters, the canonical long terminal repeat (LTR) promoter, containing three consensus AP-1 binding sites, and an internal promoter (IP) within the env gene. We investigated the regulation of the two promoters in lytic and persistent infections and found that in the presence of a constitutive source of the viral transactivator protein Tas, transactivation of the LTR promoter and that of the IP differ. In lytic infections, both the LTR promoter and the IP are efficiently transactivated by Tas, while in persistent infections, the IP is efficiently transactivated by Tas, but the LTR promoter is not. Analysis of proteins expressed from the LTR promoter and the IP during infection indicated that IP transcription is more robust than that of the LTR promoter in persistently infected cells, while the opposite is true for lytically infected cells. Coculture experiments also showed that LTR promoter transcription is greatest in cells which support lytic replication. Replacement of much of the LTR promoter with the IP leads to increased viral replication in persistent but not lytic infections. We also found that the induction of persistently infected cells with phorbol 12-myristate 13-acetate (PMA) greatly enhanced viral replication and transcription from the SFVcpz(hu) (new name for human FV) LTR promoter. However, mutation of three consensus AP-1 binding sites in the FV LTR promoter did not affect viral replication in lytically or persistently infected cells, nor did the same mutations affect LTR promoter transactivation by Tas in PMA-treated cells. Our data indicate that differential regulation of transcription is important in the outcome of FV infection but is unlikely to depend on AP-1.

* 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.

Journal of Virology, July 2001, p. 6547-6557, Vol. 75, No. 14
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.14.6547-6557.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:

  • Murray, S. M., Picker, L. J., Axthelm, M. K., Hudkins, K., Alpers, C. E., Linial, M. L. (2008). Replication in a Superficial Epithelial Cell Niche Explains the Lack of Pathogenicity of Primate Foamy Virus Infections. J. Virol. 82: 5981-5985 [Abstract] [Full Text]  
  • Murray, S. M., Picker, L. J., Axthelm, M. K., Linial, M. L. (2006). Expanded Tissue Targets for Foamy Virus Replication with Simian Immunodeficiency Virus-Induced Immunosuppression. J. Virol. 80: 663-670 [Abstract] [Full Text]  
  • Cummins, J. E. Jr., Boneva, R. S., Switzer, W. M., Christensen, L. L., Sandstrom, P., Heneine, W., Chapman, L. E., Dezzutti, C. S. (2005). Mucosal and Systemic Antibody Responses in Humans Infected with Simian Foamy Virus. J. Virol. 79: 13186-13189 [Abstract] [Full Text]  
  • Schiffer, C., Lecellier, C.-H., Mannioui, A., Felix, N., Nelson, E., Lehmann-Che, J., Giron, M.-L., Gluckman, J. C., Saib, A., Canque, B. (2004). Persistent Infection with Primate Foamy Virus Type 1 Increases Human Immunodeficiency Virus Type 1 Cell Binding via a Bet-Independent Mechanism. J. Virol. 78: 11405-11410 [Abstract] [Full Text]  
  • Kido, K., Bannert, H., Gronostajski, R. M., Flugel, R. M. (2003). Bel1-mediated Transactivation of the Spumaretroviral Internal Promoter Is Repressed by Nuclear Factor I. J. Biol. Chem. 278: 11836-11842 [Abstract] [Full Text]  
  • Lecellier, C.-H., Vermeulen, W., Bachelerie, F., Giron, M.-L., Saib, A. (2002). Intra- and Intercellular Trafficking of the Foamy Virus Auxiliary Bet Protein. J. Virol. 76: 3388-3394 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»