INDUCTION OF PRIMED T LYMPHOCYTES AND PROTECTION AGAINST FRIEND MURINE LEUKEMIA BY A RECOMBINANT VACCINIA VIRUS EXPRESSING THE FRIEND RETROVIRUS ENVELOPE GENE NLM AIDSLINE Important note: Information in this article was accurate in 1988. The state of the art may have changed since the publication date.

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INDUCTION OF PRIMED T LYMPHOCYTES AND PROTECTION AGAINST FRIEND MURINE LEUKEMIA BY A RECOMBINANT VACCINIA VIRUS EXPRESSING THE FRIEND RETROVIRUS ENVELOPE GENE

Vaccines 87. Modern Approaches to New Vaccines: Prevention of AIDS and Other Viral, Bacterial, and Parasitic Diseases. Chanock RM et al, eds. New York, Cold Spring Harbor Laboratory, p. 268-72, 1987.. Unique Identifier : AIDSLINE ICDB/88647990
Morrison RP; Chesebro B; Nishio J; Wehrly K; Earl P; Moss B; Lab. of Persistent Viral Diseases, NIAID, Rocky Mountain; Laboratories, Hamilton, MT 59840

Abstract: The discovery that members of the retrovirus family cause human leukemia and acquired immune deficiency syndrome (AIDS) has generated an interest in the development of vaccines against retroviruses. The murine model of leukemia caused by the Friend virus complex (FV) was chosen to study the potential for immune protection by using a vaccinia-retrovirus recombinant. FV causes an erythroleukemia when injected into immunocompetent adult mice. Protective immunization against FV may involve immune responses directed at surface-expressed viral antigens and repeated immunization with purified viral envelope protein has resulted in protection against lethal challenge. The gp85 product of the Friend murine leukemia virus (F-MLV) env gene is found on both virion and infected cell surfaces. Therefore, a recombinant vaccinia virus capable of expressing the gp85 product of the F-MLV env gene was chosen and investigated to determine whether protection could be achieved by vaccination with this recombinant. The entire env gene of F-MLV was placed under control of the P7.5 promoter and inserted into the thymidine kinase locus of the vaccinia virus genome. Because of the strong influence of the major histocompatibility complex (H-2) genes on spontaneous recovery from FV leukemia, testing used congenic H-2a/b (B10.A X A.BY)F1 mice and H-2a/a (B10.A X A/WySn) mice, which differ in susceptibility to FV leukemia. Both mouse strains were protected by previous infection with live N-tropic FV. Near complete protection was observed in male and female H-2a/b mice immunized by tail-scratch scarification with the vaccinia-F-MLV env recombinant virus, whereas H-2a/a mice were not protected by this immunization. Thus, genes of the H-2 complex appeared to have a profound effect on the ability to immunize protectively with the vaccinia-F-MLV env recombinant virus. Ip immunization of H-2a/b mice protected females better than males, whereas this difference was not observed when H-2a/b mice were immunized by tail-scratch scarification. Comparison of FV-specific immune parameters before and after challenge in protected and unprotected groups of mice suggested that the vaccinia-F-MLV env recombinant induced protection by priming T-lymphocyte populations to FV envelope antigens, which led to a rapid virus-specific anamnestic response. (6 Refs)
Keywords: Animal Antibodies, Viral/ANALYSIS Friend Virus/GENETICS/IMMUNOLOGY Leukemia, Experimental/*IMMUNOLOGY/PREVENTION & CONTROL Lymphocyte Transformation Mice Neutralization Tests Recombination, Genetic Retroviridae Proteins/IMMUNOLOGY T-Lymphocytes/*IMMUNOLOGY Vaccines, Synthetic/*IMMUNOLOGY Vaccinia Virus/*IMMUNOLOGY Viral Envelope Proteins/GENETICS/*IMMUNOLOGY Viral Vaccines/*IMMUNOLOGY MEETING PAPER

KWDanimalantibodies,viral/analysisfriendvirus/genetics/immunologyleukemia,experimental/KWDimmunology/prevention&controllymphocytetransformationmiceneutralizationtestsrecombination,geneticretroviridaeproteins/immunologyt-lymphocytes/KWDimmunologyvaccines,synthetic/KWDimmunologyvacciniavirus/KWDimmunologyviralenvelopeproteins/genetics/KWDimmunologyviralvaccines/KWDimmunologymeetingpaper
881130
M88B0606

Copyright © 1988 - National Library of Medicine. Reproduced under license with the National Library of Medicine, Bethesda, MD.

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