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Abstract
Background The gut mucosal homing integrin receptor a4b7 present on activated CD4+ T-cells interacts with the HIV-1 gp120 second variable loop (V2). Case control analysis of the RV144 phase III vaccine trial showed that antibodies induced by the vaccine bound to a MuLV-gp70 scaffolded V1V2 loop of gp120 (V1V2-gp70) and correlated inversely with infection. These, and other data, generate the hypothesis that the vaccine-elicited antibodies may have been involved in limiting HIV-1 acquisition. We have developed a high-throughput assay to evaluate antibodies that block a4b7 binding. We have named this the RAP assay.
Highlights
The gut mucosal homing integrin receptor a4b7 present on activated CD4+ T-cells interacts with the HIV-1 gp120 second variable loop (V2)
Plasma and purified IgG antibodies from RV144 volunteers, conformational mAbs specific for V2 (697), for V2 and V3 (PG9, PG16), or for V2 linear epitopes (CH58 and CH59, cloned from RV144 vaccinee B cells) were added to the peptide-coated plates followed by RPMI8866 cells, which constitutively express a4b7
ACT-1 inhibited the binding of both MAdCAM-1 and cyclic-V2 peptides to a4b7 by 65-85%, while CH58 and
Summary
The gut mucosal homing integrin receptor a4b7 present on activated CD4+ T-cells interacts with the HIV-1 gp120 second variable loop (V2). Case control analysis of the RV144 phase III vaccine trial showed that antibodies induced by the vaccine bound to a MuLV-gp scaffolded V1V2 loop of gp120 (V1V2-gp70) and correlated inversely with infection. These, and other data, generate the hypothesis that the vaccine-elicited antibodies may have been involved in limiting HIV-1 acquisition. We have developed a high-throughput assay to evaluate antibodies that block a4b7 binding.
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