Literature DB >> 12218150

Opsonization of HIV-1 by semen complement enhances infection of human epithelial cells.

Hicham Bouhlal1, Nicolas Chomont, Nicole Haeffner-Cavaillon, Michel D Kazatchkine, Laurent Belec, Hakim Hocini.   

Abstract

In the present study we demonstrate that both X4- and R5-tropic HIV-1 strains are able to infect the human epithelial cell line HT-29. Infection was enhanced 2-fold when HIV was added to semen before contact with the cell cultures. The enhancing effect of semen was complement dependent, as evidenced by blockage of generation of C3a/C3a(desArg) in semen by heat or EDTA treatment of semen and suppression of semen-dependent enhancement with mAbs directed to complement receptor type 3 (CD11b/CD18) and soluble CD16. Infection of HT-29 cells was assessed by the release of p24 Ag in cultures and semiquantitative PCR of the HIV-1 pol gene. Inhibition of infection of HT-29 by stromal cell-derived factor 1 was decreased in the case of semen-opsonized X4- and R5-tropic virus compared with unopsonized virus. In contrast, inhibition of infection by RANTES was increased for opsonized X4-tropic HIV-1 compared with unopsonized virus. Taken together these observations indicate that activation of complement in semen may play an enhancing role in mucosal transmission of HIV-1 by facilitating infection of epithelial cells and/or enhancing infection of complement receptor-expressing target cells in the mucosa.

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Year:  2002        PMID: 12218150     DOI: 10.4049/jimmunol.169.6.3301

Source DB:  PubMed          Journal:  J Immunol        ISSN: 0022-1767            Impact factor:   5.422


  36 in total

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Review 4.  Contraceptive methods and risk of HIV acquisition or female-to-male transmission.

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7.  Differential activity of candidate microbicides against early steps of HIV-1 infection upon complement virus opsonization.

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9.  Human seminal plasma abrogates the capture and transmission of human immunodeficiency virus type 1 to CD4+ T cells mediated by DC-SIGN.

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Review 10.  Complement and its role in protection and pathogenesis of flavivirus infections.

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