HIV-1 gp 120 blocks jacalin-induced proliferative response in CD4+ T cells: jacalin as a useful surrogate marker for qualitative and quantitative deficiency of CD4+ T cells in HIV-1 infection.

Jacalin is a plant lectin that induces mitogenic responses selectively in CD4+ T lymphocytes and has been shown to block infection by the human immunodeficiency virus type 1 (HIV-1) in a T lymphoid cell line, but the relationship of jacalin to the HIV envelope glycoprotein gp 120 in its interaction with the CD4 molecule is unclear. Here we demonstrate that pretreatment of normal T cells with native HIV-1 gp 120 impairs their ability to proliferate and secrete IL-2 in response to jacalin. This effect was not observed with deglycosylated gp 120, which fails to bind to CD4 molecule, or with gp 120 that has been premixed with soluble CD4. Flow cytometric studies and Western blotting analysis indicated that gp 120 and jacalin compete with each other in binding to CD4 molecules. In HIV-infected patients, proliferative responses of PBMC in response to jacalin were found to correlate quantitatively with percentages of CD4+ T cells but also showed a qualitative defect in comparison to healthy volunteers based on responses that were correlated for CD4+ T cell numbers. These findings suggest that (i) gp 120 and jacalin compete with each other for CD4 binding and (ii) jacalin might be a useful surrogate marker for quantitative as well as qualitative deficiency of CD4+ T cells in HIV-1 infection.