CONTRASTING IGA AND IGG NEUTRALIZATION CAPACITIES AND RESPONSES TO HIV TYPE-1 GP120 V3 LOOP IN HIV-INFECTED INDIVIDUALS

Quantitative analysis for HIV-l-specific antibodies present in IgA and IgG preparations purified from the serum of HIV-seropositive individu als indicated that the proportion of HIV-specific antibodies present w ithin the IgG isotype was seven times greater than the proportion of I gA HIV antibodies present within the IgA isotype. Dilution of IgA HIV- specific antibodies by nonspecific IgA was observed in patients with e levated serum IgA concentrations, whereas proportions of IgG HIV antib odies rose with increases in concentrations of serum IgG. Although pro portions of IgA HIV antibodies were not observed to correlate with the CD4 counts of the individuals from whom immunoglobulins were purified , a significant association between the numbers of such cells and prop ortion of HIV antibodies present in the IgG isotype was found. Equival ent amounts of IgG were also more effective than IgA at inhibiting HIV -1(IIIB) infection of a susceptible T cell line. This may be due to th e presence of higher proportions of IgG antibodies directed toward non -V3 determinants because reactivity against an HIV-1(IIIB) V3 peptide was low and did not differ significantly between these isotopes. IgA a ntibodies reacting against a V3 peptide containing the HIV consensus s equence could be detected in the majority of IgA samples purified from infected individuals. Proportions of IgG consensus V3-specific antibo dies within the purified IgG samples were, however, much higher. The p resence of accompanying increases in serum IgG concentration and propo rtions of IgG HN antibodies, higher proportions of both HIV- and conse nsus V3-specific antibodies within this isotype, and more effective ne utralization by IgG suggests that an HIV-driven response is dominated by B cells committed to production of this immunoglobulin isotype. The observed low proportions of HIV antigen-specific IgA antibodies with dilution in many individuals by elevations in non-HIV-specific IgA sug gests that IgA B cells may be more susceptible to factors that mediate the polyclonal activation believed to be responsible for many of the B cell disorders characteristic of HIV infection.