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 categories), were analyzed for total IgG, IgA, albumin (HSA), IgG, and IgA antibodies to env-encoded surface glycoproteins of HIV-1 (gp160) and of HIV-2 (gp105), by comparison to 15 age-matched healthy controls. Secretion rates of IgG and IgA into CVS were evaluated by calculation of their relative coefficients of excretion (RCE) by reference to HSA. Cervicovaginal production of anti-HIV antibodies was evaluated by comparison between specific antibody activities of IgG and of IgA to HIV in CVS were, 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 rates were normal in HIV-2-infected women. In HIV-1- but not in HIV-2-infected women, HSA levels in cervicovaginal washings were twofold increased, demonstrating alteration of the mucosal barrier in HIV-1 infection. In HIV-1-infected patients, IgG and IgA to gp160 were detected in all sera and CVS. In HIV-2-infected patients, IgG to gp105 was detected 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 IgA to HIV-1 or HIV-2 against the surface glycoprotein of the other HIV type 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 gp105 were higher in CVS than in sera, evidencing a possible local synthesis of both isotypes in HIV-1 as well as in HIV-2 infections. As early as the asymptomatic stages, HIV-1 affects the cervicovaginal mucosa more than HIV-2 does, suggesting higher viral replication within the female genital tract in HIV-1 infection than in HIV-2 infection.
Bélec
L
L
Unité d'Immunologie Microbienne, Institut Pasteur, Paris, France.
Tévi-Bénissan
C
C
Dupré
T
T
Mohamed
A S
AS
Prazuck
T
T
Gilquin
J
J
Kanga
J M
JM
Pillot
J
J
D000328:Adult; D002584:Cervix Uteri / Q000276:immunology* / Q000378:metabolism; D005260:Female; D015686:Gene Products, env / Q000276:immunology; D015483:HIV Antibodies / Q000096:biosynthesis* / Q000097:blood; D019302:HIV Envelope Protein gp160 / Q000276:immunology; D015658:HIV Infections / Q000145:classification / Q000276:immunology*; D015497:HIV-1 / Q000276:immunology*; D015498:HIV-2 / Q000276:immunology*; D006801:Humans; D007070:Immunoglobulin A / Q000096:biosynthesis* / Q000097:blood; D007074:Immunoglobulin G / Q000096:biosynthesis* / Q000097:blood; D008875:Middle Aged; D012709:Serum Albumin / Q000032:analysis; D014621:Vagina / Q000276:immunology* / Q000378:metabolism; D054299:env Gene Products, Human Immunodeficiency Virus
D015686:Gene Products, env; D015483:HIV Antibodies; D019302:HIV Envelope Protein gp160; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D012709:Serum Albumin; D054299:env Gene Products, Human Immunodeficiency Virus; C069790:gp105 envelope protein, Human immunodeficiency virus 2