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1994-10-25
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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
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).