Document 3231
 DOCN  M94A3231
 TI    Coselection in AIDS pathogenesis.
 DT    9412
 AU    Hoffmann GW; Immune Network Research Ltd., Vancouver, Canada.
 SO    Int Conf AIDS. 1994 Aug 7-12;10(1):123 (abstract no. PA0111). Unique
       Identifier : AIDSLINE ICA10/94369344
 AB    A model of AIDS pathogenesis in the context of an idiotypic network
       model is presented. Many phenomena related to AIDS have been described.
       It is important that we formulate and develop a conceptual model that
       can account for as wide a variety of the phenomena as possible.
       Phenomena to be explained include the prevalence of autoimmune phenomena
       in AIDS, the high rate of mutations observed in HIV, the fact that it
       appears to be very difficult to superinfect an animal or a culture with
       a second strain of SIV or HIV, and the fact that immunity to MHC class
       II can be protective. We postulate that the T cell receptor is involved
       in the cell infection process. A pathogenesis model is presented that is
       based on coselection (mutual positive selection) of HIV and helper T
       cells. Immune recognition of a particular viral strain favours infection
       by that strain and the selection of that strain. HIV variants that are
       recognized by as many T cells as possible are preferentially selected.
       Simultaneously, helper T cells with specificity for HIV are stimulated
       and postively selected. This is turn favours the selection of suppressor
       T cells with idiotypes that resemble HIV. Then immunity against HIV
       automatically zeroes in on the centre-pole idiotypic determinants of
       suppressor T cells. It has been found that immunity to class II MHC can
       be protective. This phenomenon will be discussed in the context of the
       coselection model. Anti-class II MHC immunity could displace the
       centre-pole, and lead to a decrease in the level of complementarity
       between helper cell idiotypes and HIV, which in turn could result in
       inhibition of infection.
 DE    Acquired Immunodeficiency Syndrome/*IMMUNOLOGY  Animal  Human
       HIV/GENETICS/*PATHOGENICITY  HLA-D Antigens/IMMUNOLOGY  *Models,
       Biological  Mutation  SIV/PATHOGENICITY
       T-Lymphocytes/*IMMUNOLOGY/MICROBIOLOGY  T-Lymphocytes,
       Helper-Inducer/IMMUNOLOGY  T-Lymphocytes, Suppressor-Effector/IMMUNOLOGY
       Variation (Genetics)  MEETING ABSTRACT

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       protected by Copyright Law (Title 17, U.S.Code).