Antisperm antibodies in human immunodeficiency virus infection: effects on fertilization and embryonic development |
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Authors: | R K Naz M Ellaurie T M Phillips J Hall |
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Institution: | Department of Obstetrics and Gynecology, Albert Einstein College of Medicine, Bronx, New York 10461. |
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Abstract: | Sera from human immunodeficiency virus (HIV)-infected males (n = 10) and females (n = 5) were analyzed for the presence of antisperm antibodies reacting against sperm-specific antigens. Of the HIV-positive males tested, sera of 40% were positive for human sperm extract (HSE), 70% for protamine, and 70% for fertilization antigen (FA-1) for at least one class of antibodies, compared to sera from HIV-negative males. Of the HIV-positive females tested, sera of 40% were positive for HSE, 30% for protamine, and 30% for FA-1 compared to sera from HIV-negative females. The majority of the sperm antigen-reactive antibodies belonged to the IgG class. The reactions observed with FA-1 were weaker than those with other antigens. Ninety percent of HIV-positive male sera and 80% of the HIV-negative female sera were found to contain immune complexes, 20% of which showed the presence of FA-1. HIV-positive male or female sera did not bind to any specific protein on the Western blot of HSE. The minimal amount of free anti-FA-1 antibodies present in sera did not bind to live sperm in the sperm immobilization technique, sperm agglutination technique, or immunobead binding technique and thus were incapable of affecting human sperm penetration of zona-free hamster ova (SPA). Nor did HIV-positive sera induce any apparent abnormality in the development of 2-cell embryos to blastocysts in vitro in murine bioassay. In conclusion, these results indicate that HIV-infected patients have sperm-specific antibodies in their sera that do not adversely affect SPA and murine embryo bioassay. There was a high incidence of immune complex formation after HIV infection. These data will provide the basis for exploring further the role of sperm antigens in altering the immunoregulatory mechanisms after HIV infection. |
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