Anecdotal descriptions of atypical FeLV infections, wherein standard clinical ELISA or immunofluorescence testing fails to detect active infections, suggest that an unknown proportion of FeLV-infected cats may go undetected. In this study, 127 viremic and nonviremic cats experimentally inoculated with FeLV were evaluated at necropsy for atypical expression of FeLV antigen. Results from viremic cats were in accordance with results of earlier studies on the pathogenesis of FeLV infection in cats, wherein antigen was found in lymphoid and epithelial tissues. Differences in time course or tissue distribution of viral antigen in some cats appeared to be attributable to the challenge virus preparations, consisting of cell-free tumor homogenate or infectious plasma. It was discovered that 5 of 19 of the FeLV challenge-exposed cats that were nonviremic had FeLV-specific antigens in select tissues (bone marrow, spleen, lymph node, and small intestine) 6 to 75 weeks after inoculation. These results indicated an additional category of possible outcomes for cats exposed to FeLV. Localized FeLV infection, as described here, may explain the discordance between clinical disease and laboratory testing for FeLV.

Bone marrow fibroblast colony-forming units (CFU-F) were evaluated in cats experimentally infected with different isolates of FeLV. Cats infected with the Kawakami-Theilen isolate of FeLV (FeLV-KT) had progressive decrease in the number of CFU-F at 2, 4, and 6 weeks after infection. The number of CFU-F in FeLV-KT-infected cats ranged from 38 to 70% of the preinoculation CFU-F value. Of 3 cats with FeLV-KT-induced suppression of CFU-F, 2 developed fatal nonregenerative anemia. Cats infected with the Rickard isolate of FeLV (FeLV-R) had more moderate decrease in the number of CFU-F at 2, 4, and 6 weeks after infection. The number of CFU-F in FeLV-R-infected cats ranged from 62 to 82% of the preinoculation CFU-F value. The FeLV-R-infected cats did not become anemic.

Phosphonoformate (PFA), a noncompetitive inhibitor of reverse transcriptase (RT), inhibited feline leukemia virus FeLV) infection of 2 feline cell lines and inhibited progeny virus RT activity in a chronically FeLV-infected cell line. Feline leukemia virus infection of 3201 cells, an FeLV-negative lymphoma cell line, was inhibited by > 70% at a concentration of only 1 micromole PFA and by > 90% at concentrations of 64 to 256 micromole PFA, as evidenced by RT activity. However, FeLV antigen expression by 3201 cells remained relatively constant over noncytotoxic concentrations of PFA. Because the persistence of viral antigen expression with concomitant suppression of RT activity appears to be unique and because 3201 cells express small amounts of an endogenous retrovirus (RD and 114) contain endogenous FeLV proviral sequences, a possible role of endogenous retroviruses acting as helper viruses was suggested. Feline leukemia virus infection of 81C cells, a sarcoma-positive, leukemia-negative fibroblast cell line, was inhibited by > 50% at a concentration of 64 micromole PFA and by > 98% at concentrations of 256 to 512 micromole PFA, as indicated by suppression of focus formation. The feline lymphoid cell line FL-74 is a large producer of FeLV. When FL-74 cells were cultured in the presence of 256 micromole PFA, virus production (virus budding and viral antigen) was not affected, but progeny virus lost RT activity and infectivity. Direct addition of PFA (256 micromole to FeLV also reduced RT activity and infectivity. These data indicate that PFA can directly and rapidly inactivate retrovirus independent of cellular processing, presumably by inhibiting RT. Long-term PFA administration may curtail spread of retroviral infections within and between hosts via extracellular inactivation of newly produced virus particles. Results of this study also suggest that PFA might be used prophylactically to treat materials potentially contaminated with retroviruses.

Biological effects of staphylococcal protein A (SPA) immunotherapy were studied in 5 viremic and 6 nonviremic cats with induced FeLV infection and in 6 control cats. The SPA therapy neither reversed FeLV viremia nor resulted in consistent improvement in humoral immune responses to FELV antigens. However, SPA immunotherapy induced a proliferative response in bone marrow granulocytic lineage, possibly resulting in expression of FeLV-free mature neutrophils in the blood. Seemingly, viral burden and chemiluminescent responses were reversed in viremic cats during SPA immunotherapy.