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Journal of Virology, July 2000, p. 5796-5801, Vol. 74, No. 13
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Differential Pathogenicity of Two Feline Leukemia Virus Subgroup A Molecular Clones, pFRA and pF6A

Andrew J. Phipps,1,2 Hang Chen,3 Kathleen A. Hayes,1,2 Pradip Roy-Burman,3,4 and Lawrence E. Mathes1,2,5,*

Department of Veterinary Biosciences,1 Center for Retrovirus Research,2 and Comprehensive Cancer Center,5 The Ohio State University, Columbus, Ohio 43210, and Departments of Pathology4 and Biochemistry and Molecular Biology,3 University of Southern California School of Medicine, Los Angeles, California 90033

Received 6 December 1999/Accepted 29 March 2000

F6A, a molecular clone of subgroup A feline leukemia virus (FeLV) is considered to be highly infectious but weakly pathogenic. In recent studies with a closely related subgroup A molecular clone, FRA, we demonstrated high pathogenicity and a strong propensity to undergo recombination with endogenous FeLV (enFeLV), leading to a high frequency of transition from subgroup A to A/B. The present study was undertaken to identify mechanisms of FeLV pathogenesis that might become evident by comparing the two closely related molecular clones. F6A was shown to have an infectivity similar to that of FRA when delivered as a provirus. Virus load and antibody responses were also similar, although F6A-infected cats consistently carried higher virus loads than FRA-infected cats. However, F6A-infected cats were slower to undergo de novo recombination with enFeLV and showed slower progression to disease than FRA-infected cats. Tumors collected from nine pF6A- or pFRA-inoculated cats expressed lymphocyte markers for T cells (seven tumors) and B cells (one tumor), and non-T/B cells (one tumor). One cat with an A-to-A/C conversion developed erythrocyte hypoplasia. Genomic mapping of recombinants from pF6A- and pFRA-inoculated cats revealed similar crossover sites, suggesting that the genomic makeup of the recombinants did not contribute to increased progression to neoplastic disease. From these studies, the mechanism most likely to account for the pathologic differences between F6A and FRA is the lower propensity for F6A to undergo de novo recombination with enFeLV in vivo. A lower recombination rate is predicted to slow the transition from subgroup A to A/B and slow the progression to disease.

* Corresponding author. Mailing address: The Ohio State University, Center for Retrovirus Research, 1925 Coffey Rd., Columbus, OH 43210. Phone: (614) 292-7317. Fax: (614) 292-6473. E-mail: mathes.2{at}osu.edu.

Journal of Virology, July 2000, p. 5796-5801, Vol. 74, No. 13
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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