Recombinant feline leukemia virus (FeLV) variants establish a limited infection with altered cell tropism in specific-pathogen-free cats in the absence of FeLV subgroup a helper virus

Feline leukemia virus subgroup B (FeLV-B) is commonly associated with felin e lymphosarcoma and arises through recombination between endogenous retrovi ral elements inherited in the cat genome and corresponding regions of the e nvelope (env) gene from FeLV subgroup A (FeLV-A). In vivo infectivity for F eLV-B is thought to be inefficient in the absence of FeLV-A. Proposed FeLV- A helper functions include enhanced replication efficiency, immune evasion, and replication rescue for defective FeLV-B virions. In vitro analysis of the recombinant FeLV-B-like viruses (rFeLVs) employed in this study confirm ed these viruses were replication competent prior to their use in an in viv o study without FeLV-A helper virus. Eight specific-pathogen-free kittens w ere inoculated with the rFeLVs alone. Subsequent hematology and histology r esults were within normal limits, however, in the absence of detectable vir emia, virus expression, or significant seroconversion, rFeLV proviral DNA w as detected in bone marrow tissue of 4/4 (100%) cats at 45 weeks postinocul ation (pi), indicating these rFeLVs established a limited but persistent in fection in the absence of FeLV-A. Altered cell tropism was also noted. Foca l infection was seen in T-cell areas of the splenic follicles in 3/4 (75%) rFeLV-infected cats analyzed, while an FeLV-A-infected cat showed focal inf ection in B-cell areas of the splenic follicles. Nucleotide sequence analys is of the surface glycoprotein portion of the rFeLV env gene amplified from bone marrow tissue collected at 45 weeks pi showed no sequence alterations from the original rFeLV inocula.