Author(s): Beverley PC, Healey D, Broadhurst K, Sattentau QJ
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Abstract Attempts to raise protective immunity to HIV have been notably ineffective. However the conservation of binding of different virus strains to CD4 suggests that the HIV envelope glycoprotein (gp120) should have a conserved site for CD4. Attempts to raise neutralizing anti-idiotypes to CD4 monoclonal antibodies (MoAbs) have generated polyclonal sera which block HIV-induced syncytium formation in vitro but have low titres. Mapping of CD4 epitopes recognized by CD4 MoAbs and gp120 indicates that none of the present CD4 MoAbs bind to exactly the same site as gp120, which may explain the relative lack of success of the anti-idiotype approach to date.
This article was published in J Autoimmun
and referenced in Journal of Proteomics & Bioinformatics