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. 2007 Oct 17;82(1):115–125. doi: 10.1128/JVI.00927-07

FIG. 6.

FIG. 6.

(A) Ability of plasma from 75 chronically HIV-1-positive patients (CD4 counts of >400; no antiretroviral therapy) and HIV-1-negative control plasma from 25 healthy donors to inhibit either the biotinylated MAb 2F5 or MAb 13H11. Twenty of 50 plasma samples from the chronically HIV-1-positive patients inhibited MAb 2F5 binding at ≥20% levels, while 62 of 75 plasma samples from the chronically HIV-1-positive patients inhibited MAb 13H11 binding at ≥20% levels. No significant inhibition of either MAb 2F5 or 13H11 binding by HIV-1-negative control plasma (n = 50) was observed. (B) Ability of plasma from 20 acutely HIV-1-infected patients and HIV-1-negative control plasma from 26 healthy donors to inhibit either the biotinylated MAb 2F5 or MAb 13H11. Two of 20 plasma samples from the acutely HIV-1-infected patients inhibited MAb 2F5 binding at ≥20% levels, while 19 of 20 plasma samples from the acutely HIV-1-infected patients inhibited MAb 13H11 binding at ≥20% levels. No significant inhibition of either MAb 2F5 or 13H11 binding by HIV-1-negative control plasma (n = 26) was observed. (C) Ability of plasma from 75 chronically HIV-1-positive patients (CD4 counts of >400; no antiretroviral therapy) to bind either the 2F5 epitope peptide SP62 or the 4E10 epitope peptide 4E10P in direct ELISA. A total of 23% of plasma samples from chronically HIV-1-positive patients were reactive with SP62 2F5 peptide while 8% were reactive with the 4E10 gp41 epitope peptide. Plasma samples were considered positive in peptide reactivity if the OD value was ≥0.500.