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Journal of Virology, February 2005, p. 1351-1360, Vol. 79, No. 3
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.3.1351-1360.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Subtle Mutational Changes in the SU Protein of a Natural Feline Leukemia Virus Subgroup A Isolate Alter Disease Spectrum

Chandtip Chandhasin,1,2,3 Patricia N. Coan,4 and Laura S. Levy1,2,3*

Department of Microbiology and Immunology,1 Program in Molecular and Cellular Biology,2 Tulane Cancer Center,3 Department of Vivarial Science and Research, Tulane University Health Sciences Center, New Orleans, Louisiana4

Received 20 July 2004/ Accepted 22 September 2004

FeLV-945 is a representative isolate of the natural feline leukemia virus (FeLV) variant predominant in non-T-cell malignant, proliferative, and degenerative diseases in a geographic cohort. The FeLV-945 surface glycoprotein (SU) is closely related to natural horizontally transmissible FeLV subgroup A (FeLV-A) but was found to differ from a prototype to a larger extent than the members of FeLV-A differ among themselves. The sequence differences included point mutations restricted largely to the functional domains of SU, i.e., VRA, VRB, and PRR. Despite the sequence differences in these critical domains, measurements of receptor utilization, including host range and superinfection interference, confirmed the assignment of FeLV-945 to subgroup A. Other proviruses isolated from the cohort contained similar sequence hallmarks and were assigned to FeLV subgroup A. A provirus from cat 1046 contained a histidine-to-proline change at SU residue 6 within an SPHQ motif that was previously identified as a critical mediator of fusion events during virus entry. The 1046 pseudotype virus entered cells only in the presence of the soluble cofactor FeLIX provided in trans, but it retained an ecotropic host range even in the presence of FeLIX. The mutational changes in FeLV-945 were shown to confer significant functional differences compared to prototype FeLV-A viruses. The substitution of FeLV-945 envelope gene sequences for FeLV-A/61E sequences conferred a small but statistically significant replicative advantage in some feline cells. Moreover, substitution of the unique FeLV-945 long terminal repeat and envelope gene for those of FeLV-A/61E altered the disease spectrum entirely, from a thymic lymphoma of a T-cell origin to an as yet uncharacterized multicentric lymphoma that did not contain T cells.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, Tulane University School of Medicine, 1430 Tulane Ave. SL-38, New Orleans, LA 70112. Phone: (504) 988-2083. Fax: (504) 988-5144. E-mail: llevy{at}tulane.edu.

Journal of Virology, February 2005, p. 1351-1360, Vol. 79, No. 3
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.3.1351-1360.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Finstad, S. L., Rosenberg, N., Levy, L. S. (2007). Diminished Potential for B-Lymphoid Differentiation after Murine Leukemia Virus Infection In Vivo and in EML Hematopoietic Progenitor Cells. J. Virol. 81: 7274-7279 [Abstract] [Full Text]  
  • Mendoza, R., Anderson, M. M., Overbaugh, J. (2006). A putative thiamine transport protein is a receptor for feline leukemia virus subgroup a.. J. Virol. 80: 3378-3385 [Abstract] [Full Text]  
  • Chandhasin, C., Coan, P. N., Pandrea, I., Grant, C. K., Lobelle-Rich, P. A., Puetter, A., Levy, L. S. (2005). Unique Long Terminal Repeat and Surface Glycoprotein Gene Sequences of Feline Leukemia Virus as Determinants of Disease Outcome. J. Virol. 79: 5278-5287 [Abstract] [Full Text]  


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