Important note: Information in this article was accurate in 1991. The state of the art may have changed since the publication date.
INDUCTION OF PROTECTIVE IMMUNITY AGAINST AN IMMUNOSUPPRESSIVE MOUSE RETROVIRUS: POSSIBLE PARALLELS WITH HIV
AIDS Vaccine Research and Clinical Trials. Putney SD and Bolognesi DP, eds. New York, Marcel Dekker, p. 301-18, 1990.. Unique Identifier : AIDSLINE ICDB/91676952 Chesebro B; Rocky Mountain Lab., Natl. Inst. of Allergy and Infectious; Diseases, Hamilton, MT
Abstract:
Friend virus (FV) maintains a chronic persistent infection of many cell types in vivo. Effective protective immunity should be capable of recognizing both cell-free virions and infected cells. The FV mouse model may be appropriate for studying problems of development of protective immunity that might be relevant to HIV in humans. Experiments using this model system are reviewed, including protective immunity against challenge with cell-free FV and live allogeneic virus-infected cells, mechanisms of protection, possible role of virus-induced immunosuppression as a mechanism of resistance to induction of protective immunity, protective immunization of genetic nonresponder mice, and virus carrier status of protected individuals. To analyze possible mechanisms of protection following immunization of mice, status of the virus-specific immune response of H-2a/b mice was examined prior to and after challenge with FV complex. Mice with recombinant H-2 genotypes were used to see whether a previously observed effect of H-2 genotype on induction of immune protection and the H-2 effect on virus-induced immunosuppression were mediated by the same H-2 subregions. Susceptibility to immunosuppression was mediated by the D subregion of H-2, whereas the ability to mount a protective immune response to FV challenge following immunization with vaccinia-friend murine leukemia virus env was mapped to the K or I-A subregions of H-2. One striking result of these studies was the observation that successful protective immunization usually did not block infection by challenge FV. Rather, immunization appeared to prime mice so that they could recover rapidly from splenomegaly induced by infection after challenge. In the FV model protective immunity could be induced even in the face of severe host genetic susceptibility to virus-induced immunosuppression. There was significant host genetic variability in ability to mount a protective immune response to certain immunogens. Even low-responder individuals could be immunized if immunization was done with appropriate viral antigens and immunogenic adjuvants. It is likely that host genetic variability may also have a strong influence on the immune response of different individuals to HIV antigens. Thus, it may be necessary to consider similar ways to maximally enhance the protective immune response of humans to HIV. (49 Refs)
Keywords: Animal Antibody Formation/*IMMUNOLOGY Antigenic Variation/IMMUNOLOGY Cytopathogenic Effect, Viral/IMMUNOLOGY Friend Virus/*IMMUNOLOGY Human HIV/*IMMUNOLOGY HIV Antigens/IMMUNOLOGY HIV Infections/*IMMUNOLOGY Immune Tolerance/IMMUNOLOGY Leukemia, Erythroblastic, Acute/*IMMUNOLOGY Mice Vaccines, Synthetic/*IMMUNOLOGY Viral Vaccines/*IMMUNOLOGY MONOGRAPH REVIEW 912130
M91C4090
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Important note: Information in this article was accurate in 1991. The state of the art may have changed since the publication date.
