Protection against feline leukemia virus infection by use of an inactivated virus vaccine

Edward A. Hoover From the Department of Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523 (Hoover, Perigo, Quackenbush, Mathiason-DuBard), the Department of Microbiology, School of Medicine, University of Washington, SC-42, G311 Health Sciences Building, Seattle, WA 98195 (Overbaugh), the Johnson and Johnson, Pharmaceuticals Research, Inc, PO Box 8289, LaJolla, CA 92038 (Kloetzer), the Molecular Biology Department, The Scripps Research Institute, 10666 N Torrey Pines, LaJolla, CA 92037 (Elder), and the Department of Microbiology and Immunology, Stanford University Medical Center, Sherman Fairchild Science Center, Stanford, CA 94305 (Mullins).

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Nancy A. Perigo From the Department of Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523 (Hoover, Perigo, Quackenbush, Mathiason-DuBard), the Department of Microbiology, School of Medicine, University of Washington, SC-42, G311 Health Sciences Building, Seattle, WA 98195 (Overbaugh), the Johnson and Johnson, Pharmaceuticals Research, Inc, PO Box 8289, LaJolla, CA 92038 (Kloetzer), the Molecular Biology Department, The Scripps Research Institute, 10666 N Torrey Pines, LaJolla, CA 92037 (Elder), and the Department of Microbiology and Immunology, Stanford University Medical Center, Sherman Fairchild Science Center, Stanford, CA 94305 (Mullins).

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Sandra L. Quackenbush From the Department of Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523 (Hoover, Perigo, Quackenbush, Mathiason-DuBard), the Department of Microbiology, School of Medicine, University of Washington, SC-42, G311 Health Sciences Building, Seattle, WA 98195 (Overbaugh), the Johnson and Johnson, Pharmaceuticals Research, Inc, PO Box 8289, LaJolla, CA 92038 (Kloetzer), the Molecular Biology Department, The Scripps Research Institute, 10666 N Torrey Pines, LaJolla, CA 92037 (Elder), and the Department of Microbiology and Immunology, Stanford University Medical Center, Sherman Fairchild Science Center, Stanford, CA 94305 (Mullins).

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Candace K. Mathiason-DuBard From the Department of Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523 (Hoover, Perigo, Quackenbush, Mathiason-DuBard), the Department of Microbiology, School of Medicine, University of Washington, SC-42, G311 Health Sciences Building, Seattle, WA 98195 (Overbaugh), the Johnson and Johnson, Pharmaceuticals Research, Inc, PO Box 8289, LaJolla, CA 92038 (Kloetzer), the Molecular Biology Department, The Scripps Research Institute, 10666 N Torrey Pines, LaJolla, CA 92037 (Elder), and the Department of Microbiology and Immunology, Stanford University Medical Center, Sherman Fairchild Science Center, Stanford, CA 94305 (Mullins).

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Julie M. Overbaugh From the Department of Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523 (Hoover, Perigo, Quackenbush, Mathiason-DuBard), the Department of Microbiology, School of Medicine, University of Washington, SC-42, G311 Health Sciences Building, Seattle, WA 98195 (Overbaugh), the Johnson and Johnson, Pharmaceuticals Research, Inc, PO Box 8289, LaJolla, CA 92038 (Kloetzer), the Molecular Biology Department, The Scripps Research Institute, 10666 N Torrey Pines, LaJolla, CA 92037 (Elder), and the Department of Microbiology and Immunology, Stanford University Medical Center, Sherman Fairchild Science Center, Stanford, CA 94305 (Mullins).

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William S. Kloetzer From the Department of Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523 (Hoover, Perigo, Quackenbush, Mathiason-DuBard), the Department of Microbiology, School of Medicine, University of Washington, SC-42, G311 Health Sciences Building, Seattle, WA 98195 (Overbaugh), the Johnson and Johnson, Pharmaceuticals Research, Inc, PO Box 8289, LaJolla, CA 92038 (Kloetzer), the Molecular Biology Department, The Scripps Research Institute, 10666 N Torrey Pines, LaJolla, CA 92037 (Elder), and the Department of Microbiology and Immunology, Stanford University Medical Center, Sherman Fairchild Science Center, Stanford, CA 94305 (Mullins).

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John H. Elder From the Department of Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523 (Hoover, Perigo, Quackenbush, Mathiason-DuBard), the Department of Microbiology, School of Medicine, University of Washington, SC-42, G311 Health Sciences Building, Seattle, WA 98195 (Overbaugh), the Johnson and Johnson, Pharmaceuticals Research, Inc, PO Box 8289, LaJolla, CA 92038 (Kloetzer), the Molecular Biology Department, The Scripps Research Institute, 10666 N Torrey Pines, LaJolla, CA 92037 (Elder), and the Department of Microbiology and Immunology, Stanford University Medical Center, Sherman Fairchild Science Center, Stanford, CA 94305 (Mullins).

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James I. Mullins From the Department of Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523 (Hoover, Perigo, Quackenbush, Mathiason-DuBard), the Department of Microbiology, School of Medicine, University of Washington, SC-42, G311 Health Sciences Building, Seattle, WA 98195 (Overbaugh), the Johnson and Johnson, Pharmaceuticals Research, Inc, PO Box 8289, LaJolla, CA 92038 (Kloetzer), the Molecular Biology Department, The Scripps Research Institute, 10666 N Torrey Pines, LaJolla, CA 92037 (Elder), and the Department of Microbiology and Immunology, Stanford University Medical Center, Sherman Fairchild Science Center, Stanford, CA 94305 (Mullins).

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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.

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.

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