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Selective deficit in antibodies specific for the superantigen binding site of gp120 in HIV infection


Selective deficit in antibodies specific for the superantigen binding site of gp120 in HIV infection



FASEB Journal 12(14): 1473-1480



ISSN/ISBN: 0892-6638

PMID: 9806756

HIV infection is characterized by accelerated apoptosis and progressive loss of B cells. To see whether these abnormalities are related to the property of gp120 to act as a superantigen for VH3(+) B cells, we probed the temporal development of VH3(+) antibodies in HIV-1-infected subjects over a 7-year period. We found that VH3(+) antibodies specific for the gp120 superantigen binding site are deficient. Since VH3(+) antibodies impart protective responses to infectious agents, we quantified VH3(+) antibodies in serum samples from HIV-seropositive slow progressors and from patients who progressed to AIDS-related manifestations. We found that paucity in VH3(+) antibodies is a marker of rapid clinical decline. Remarkably, anti-gp160 VH3(+) antibodies showed a gradual decrease in progressors and, with time, varied depending on the viral load. We conclude that disease aggravation is associated with a decrease of the magnitude of the humoral response, that VH3(+) antibodies play an important role in protection, and that their underexpression may accelerate disease progression. We propose that vaccine preparations able to trigger VH3(+) antibodies might confer a better protection against HIV infection. This work also represents a novel mechanism of humoral deficiency resulting from the capacity of a viral antigen to affect an important subset of the B cell repertoire and to induce B cell death by apoptosis.

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Accession: 018110160

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