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  • Author or Editor: Edward A. Hoover x
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Summary

Feline leukemia virus is a naturally occurring, contagiously transmitted and oncogenic immunosuppressive retrovirus of cats. The effects of FeLV are paradoxical, causing cytoproliferative and cytosuppressive disease (eg, lymphoma and myeloproliferative disorders vs immunodeficiency and myelosuppressive disorders). In the first few weeks after virus exposure, interactions between FeLV and hemolymphatic system cells determine whether the virus or the cat will dominate in the host/virus relationship—persistent viremia and progressive infection or self limiting, regressive infection will develop. The outcome of these early host/virus interactions is revealed in the diagnostic assays for FeLV antigenemia and viremia. The latter, in turn, predict the outcome of FeLV infection in cats. Known host resistance factors include age and immune system functional status. Known virus virulence factors are magnitude of exposure and virus genotype. Molecular analysis of FeLV strains indicated that natural virus isolates exist as mixtures of closely related virus genotypes and that minor genetic variations among FeLV strains can impart major differences in pathogenicity. The genetic coding regions responsible for cell targeting and specific disease inducing capacity (eg, thymic lymphoma, acute immunosuppression, or aplastic anemia) have been mapped to the virus surface glycoprotein and/or long terminal repeat regions for several FeLV strains. Infection by specific FeLV strains leads to either malignant transformation or cytopathic deletion of specific lymphocyte and hemopoietic cell population, changes that prefigure the onset of clinical illness. Another notable feature of the biology of FeLV is that many cats are able to effectively contain and terminate viral replication, an important example of host immunologic control of a retrovirus infection and a process that can be selectively enhanced by vaccination. Thus, FeLV infection serves as a natural model of the multifaceted pathogenesis of retroviruses and as a paradigm for immunoprophylaxis against an immunosuppressive leukemogenic retrovirus.

Free access
in Journal of the American Veterinary Medical Association

SUMMARY

We generated monoclonal antibodies (mab) against feline immunodeficiency virus (fiv) and characterized these mab by single competition enzyme immunoassays (eia), immunoblot analysis, and radioimmunoprecipitation. Four mab identified 3 distinct epitopes of the fiv p24/26 gag major core protein. One mab recognized the pl6/17 gag protein; none recognized envelope proteins. We developed an fiv p26 antigen capture eia that proved more sensitive (0.5 ng of p26/ml), less expensive, and less timeconsuming than reverse transcriptase assay. The same mab were used to develop an antibody eia specific for fiv p26. The mab and capture assays reported should prove useful in fiv diagnosis and research.

Free access
in American Journal of Veterinary Research

Summary

Immunodeficiency was diagnosed as the cause of severe debilitating disease characterized by weight loss, failure to grow, and persistent infections that failed to respond to treatment in 12 young llamas. The llamas were affected after maternal-acquired immunity had decreased; failure of passive transfer of immunoglobulins thus was not suspected. Areas of lymph nodes containing T lymphocytes were hypocellular, suggesting T-cell involvement. High serum immunoglobulin concentrations were not found, despite the existence of infectious disease, suggesting at least secondary B-cell involvement. Results of lymphocyte blastogenesis assays were suggestive of B- and T-cell involvement. It was not possible to determine whether the condition was inherited or acquired.

Free access
in Journal of the American Veterinary Medical Association

Summary

The protective immunity induced by 3 experimental FeLV vaccines were evaluated: Prototype inactivated FeLV vaccine developed from a molecularly cloned FeLV isolate (FeLV-faids-61E-A); a mixture of immunodominant synthetic peptides corresponding to regions of the FeLV-Gardner-Arnstein-B (FeLV-GA-B) envelope proteins; and an adjuvant-disrupted but non-activated virus prepared from a non-cloned FeLV field isolate comprised of subgroup A and B viruses (FeLV-05821-AB). Included as controls were parallel groups of cats inoculated with adjuvants alone or with an established commercial FeLV vaccine. After each inoculation and after virulent virus challenge exposure, sera from all cats were assayed for elisa-reactive antibody against purified FeLV, FeLV neutralizing (vn) antibody, and FeLV antigenemia/viremia—viral p27 antigen in serum and within circulating leukocytes. Immunity was challenged by oral/nasal exposure of vaccinated and control cats with FeLV-faids-61E-A or FeLV-05821-AB, an infective. noncloned, tissue-origin, FeLV field isolate containing suhgroup-A and -B viruses. Vaccine-induced immunity was assessed by comparing the postchallenge-exposure incidence of persistent viremia and the pre- and postchallenge exposure titers of vn and elisa antibody in cats of the control and vaccine groups. The percentage of cats that resisted development of persistent viremia after FeLV challenge exposure and the preventable fraclion (pf) for the vaccine groups (which adjusts for the severity of the challenge and the degree of innate resistance in the controls) were as allows: adjuvant controls, 26%; FeLV-faids-61E-A inactivated virus vaccine, 95% (pf = 93.2%); FeLV-GA-B peptide vaccine, 5% (−28.4%); FeLV- 05821-AB noninactivated vaccine, 67% (55.4%); and commercial FeLV vaccine, 35% (12.2%). The prechallenge exposure mean vn antibody titer for each group was: <1:8 in the adjuvant controls; 1:43 in the FeLV-faids-61E-A-vaccinated cats; <1:8 in the peptide-vaccinated cats; 1:38 in the noninactivated virus-vaccinated cats group; and 1:12 in the cats vaccinated with the commercial vaccine. Thus, induction of vn antibody in the vaccinated cats, although modest, appeared to be correlated with induction of protective immunity as defined by resistance to FeLV challenge exposure. Results of these studies indicate that inoculation of cats with an experimental inactivated virus vaccine prepared from a molecularly cloned FeLV isolate was most effective in stimulating protective immunity against heterologous and homologous FeLV challenge exposure.

Free access
in Journal of the American Veterinary Medical Association