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 Lauring, A. S.
Right arrow Articles by Overbaugh, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lauring, A. S.
Right arrow Articles by Overbaugh, J.

 Previous Article  |  Next Article 

Journal of Virology, October 2001, p. 8888-8898, Vol. 75, No. 19
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.19.8888-8898.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Specificity in Receptor Usage by T-Cell-Tropic Feline Leukemia Viruses: Implications for the In Vivo Tropism of Immunodeficiency-Inducing Variants

Adam S. Lauring,1,2 Maria M. Anderson,2 and Julie Overbaugh2,*

Program in Molecular and Cellular Biology, University of Washington,1 and Division of Human Biology, Fred Hutchinson Cancer Research Center,2 Seattle, Washington

Received 13 April 2001/Accepted 23 June 2001

Cytopathic, T-cell-tropic feline leukemia viruses (FeLV-T) evolve from FeLV-A in infected animals and demonstrate host cell specificities that are distinct from those of their parent viruses. We recently identified two cellular proteins, FeLIX and Pit1, required for productive infection by these immunodeficiency-inducing FeLV-T variants (M. M. Anderson, A. S. Lauring, C. C. Burns, and J. Overbaugh, Science 287:1828-1830, 2000). FeLV-T is the first example of a naturally occurring type C retrovirus that requires two proteins to gain entry into target cells. FeLIX is an endogenous protein that is highly related to the N-terminal portion of the FeLV envelope protein, which includes the receptor-binding domain. Pit1 is a multiple-transmembrane phosphate transport protein that also functions as a receptor for FeLV-B. The FeLV-B envelope gene is derived by recombination with endogenous FeLV-like sequences, and its product can functionally substitute for FeLIX in facilitating entry through the Pit1 receptor. In the present study, we tested other retrovirus envelope surface units (SUs) with their cognate receptors to determine whether they also could mediate infection by FeLV-T. Cells were engineered to coexpress the transmembrane form of the envelope proteins and their cognate receptors, or SU protein was added as a soluble protein to cells expressing the receptor. Of the FeLV, murine leukemia virus, and gibbon ape leukemia virus envelopes tested, we found that only those with receptor-binding domains derived from endogenous FeLV could render cells permissive for FeLV-T. We also found that there is a strong preference for Pit1 as the transmembrane receptor. Specifically, FeLV-B SUs could efficiently mediate infection of cells expressing the Pit1 receptor but could only inefficiently mediate infection of cells expressing the Pit2 receptor, even though these SUs are able to bind to Pit2. Expression analysis of feline Pit1 and FeLIX suggests that FeLIX is likely the primary determinant of FeLV-T tropism. These results are discussed in terms of current models for retrovirus entry and the interrelationship among FeLV variants that evolve in vivo.

* Corresponding author. Mailing address: Division of Human Biology, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., C3-168, Seattle, WA 98109-1024. Phone: (206) 667-3524. Fax: (206) 667-1535. E-mail: joverbau{at}fhcrc.org.

Journal of Virology, October 2001, p. 8888-8898, Vol. 75, No. 19
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.19.8888-8898.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:

  • Argaw, T., Figueroa, M., Salomon, D. R., Wilson, C. A. (2008). Identification of Residues outside of the Receptor Binding Domain That Influence the Infectivity and Tropism of Porcine Endogenous Retrovirus. J. Virol. 82: 7483-7491 [Abstract] [Full Text]  
  • Sarangi, A., Bupp, K., Roth, M. J. (2007). Identification of a retroviral receptor used by an Envelope protein derived by peptide library screening. Proc. Natl. Acad. Sci. USA 104: 11032-11037 [Abstract] [Full Text]  
  • Rodenburg, M., Fischer, M., Engelmann, A., Harbers, S. O., Ziegler, M., Lohler, J., Stocking, C. (2007). Importance of Receptor Usage, Fli1 Activation, and Mouse Strain for the Stem Cell Specificity of 10A1 Murine Leukemia Virus Leukemogenicity. J. Virol. 81: 732-742 [Abstract] [Full Text]  
  • Oliveira, N. M., Farrell, K. B., Eiden, M. V. (2006). In Vitro Characterization of a Koala Retrovirus. J. Virol. 80: 3104-3107 [Abstract] [Full Text]  
  • Cheng, H. H., Anderson, M. M., Hankenson, F. C., Johnston, L., Kotwaliwale, C. V., Overbaugh, J. (2006). Envelope Determinants for Dual-Receptor Specificity in Feline Leukemia Virus Subgroup A and T Variants. J. Virol. 80: 1619-1628 [Abstract] [Full Text]  
  • Chandhasin, C., Coan, P. N., Levy, L. S. (2005). Subtle Mutational Changes in the SU Protein of a Natural Feline Leukemia Virus Subgroup A Isolate Alter Disease Spectrum. J. Virol. 79: 1351-1360 [Abstract] [Full Text]  
  • Lavillette, D., Kabat, D. (2004). Porcine Endogenous Retroviruses Infect Cells Lacking Cognate Receptors by an Alternative Pathway: Implications for Retrovirus Evolution and Xenotransplantation. J. Virol. 78: 8868-8877 [Abstract] [Full Text]  
  • Feldman, S. A, Farrell, K. B., Murthy, R. K., Russ, J. L., Eiden, M. V. (2004). Identification of an Extracellular Domain within the Human PiT2 Receptor That Is Required for Amphotropic Murine Leukemia Virus Binding. J. Virol. 78: 595-602 [Abstract] [Full Text]  
  • Barnett, A. L., Wensel, D. L., Li, W., Fass, D., Cunningham, J. M. (2003). Structure and Mechanism of a Coreceptor for Infection by a Pathogenic Feline Retrovirus. J. Virol. 77: 2717-2729 [Abstract] [Full Text]  
  • Faix, P. H., Feldman, S. A., Overbaugh, J., Eiden, M. V. (2002). Host Range and Receptor Binding Properties of Vectors Bearing Feline Leukemia Virus Subgroup B Envelopes Can Be Modulated by Envelope Sequences outside of the Receptor Binding Domain. J. Virol. 76: 12369-12375 [Abstract] [Full Text]  
  • Lauring, A. S., Cheng, H. H., Eiden, M. V., Overbaugh, J. (2002). Genetic and Biochemical Analyses of Receptor and Cofactor Determinants for T-Cell-Tropic Feline Leukemia Virus Infection. J. Virol. 76: 8069-8078 [Abstract] [Full Text]  
  • Farrell, K. B., Russ, J. L., Murthy, R. K., Eiden, M. V. (2002). Reassessing the Role of Region A in Pit1-Mediated Viral Entry. J. Virol. 76: 7683-7693 [Abstract] [Full Text]  
  • Farrell, K. B., Ting, Y.-T., Eiden, M. V. (2002). Fusion-Defective Gibbon Ape Leukemia Virus Vectors Can Be Rescued by Homologous but Not Heterologous Soluble Envelope Proteins. J. Virol. 76: 4267-4274 [Abstract] [Full Text]  
  • Anderson, M. M., Lauring, A. S., Robertson, S., Dirks, C., Overbaugh, J. (2001). Feline Pit2 Functions as a Receptor for Subgroup B Feline Leukemia Viruses. J. Virol. 75: 10563-10572 [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»