COMPARISON OF CERVICOVAGINAL HUMORAL IMMUNITY IN CLINICALLY ASYMPTOMATIC (CDC A1 AND A2 CATEGORY) PATIENTS WITH HIV-1 AND HIV-2 INFECTION

Paired sera and cervicovaginal secretions (CVS) from 11 HIV-1- and 11 HIV-2-infected women, all clinically asymptomatic (CDC A1 and A2 categ ories), were analyzed for total IgC. IgA, albumin (HSA), IgG, and IgA antibodies to env-encoded surface glycoproteins of HIV-1 (gp 160) and of HIV-2 (gp105), by comparison to 15 age-matched healthy controls. Se cretion rates of IgG and IgA into CVS were evaluated by calculation of their relative coefficients of excretion (RCE) by reference to HSA. C ervicovaginal production of anti-HIV antibodies was evaluated by compa rison between specific antibody activities of IgG and of IgA to HIV in CVS and in sera. In HIV-1-infected women, total IgG and IgA in CVS we re, respectively, 6- and 4-fold increased, whereas the secretion rate of total IgG was 2.1-fold increased and that of total IgA was 2.5-fold reduced. In contrast, total IgG and IgA as well as their secretion la res were normal in HIV-2-infected women. In HIV-1- but not in HIV-2-in fected women, HSA levels in cervicovaginal washings were twofold incre ased, demonstrating alteration of the mucosal barrier in HIV-1 infecti on. In HIV-1-infected patients, IgG and IgA to gp160 were detected in ail sera and CVS. In HIV-2-infected patients, IgG to gp105 was detecte d in all sera and CVS, whereas IgA to gp105 could be detected in only half of sera and one-third of CVS. Cross-reactivity by IgG and/or ISA to HIV-1 or HIV-2 against the surface glycoprotein of the other HIV ty pe was observed in sera as well as in CVS, and more frequently in HIV- 2- than in HIV-1-infected women. Finally, the mean specific activities of IgG and of IgA to gp160 or gp 105 were higher in CVS than in sera, evidencing a possible local synthesis of both isotypes in HIV-1 as we ll as in HIV-2 infections. As early as the asymptomatic stages, HIV-1 affects the cervicovaginal mucosa more than HIV-2 does, suggesting hig her viral replication within the female genital tract in HIV-1 infecti on than in HIV-2 infection.