J Infect Dis
August 2003
Using ultrasensitive polymerase chain reaction-based techniques, we assessed levels of cell-free and cell-associated human immunodeficiency virus (HIV)-1 in paired blood and genital samples of 30 clinically asymptomatic, treatment-naive women. Levels of HIV-1 RNA in cervicovaginal-lavage samples were positively correlated with those in plasma samples (r=.50; P=.
View Article and Find Full Text PDFMost cases of human immunodeficiency virus (HIV) infection worldwide occur following sexual contact, implying that the virus may breach the protective epithelial barrier lining the genital tract. HIV infection is known to preferentially occur when the genital epithelial integrity is altered, particularly when epithelial micro-ulcerations occur during heterosexual intercourse or ulcerations appear, due to sexually transmitted infections or else in the context of ectopy of the endocervical mucosa, which may leave the genital tissue. We report that R5-tropic infectious HIV-1 isolates are capable of in vitro transcytosis through a tight and polarized monolayer of human endometrial HEC-1 cells.
View Article and Find Full Text PDFThe search for heparin-like materials remains an intensive field of research. In this context, we studied the immunomodulatory properties of semisynthetic dextran derivatives and naturally occurring sulfated polysaccharides present in brown seaweed (fucans). In this study, we investigated the functional potencies of fucan and dextran derivatives by analyzing their effects on the release of proinflammatory cytokines by resting or lipopolysaccharide (LPS)-stimulated human monocytes and their interactions on monocyte surfaces.
View Article and Find Full Text PDFTransmigration of human immunodeficiency virus (HIV)-infected mononuclear cells through the genital mucosa is one of the possible mechanisms of sexual transmission of HIV. Here, we investigated the transmigration of cell-associated R5-tropic HIV type 1 (HIV-1) through a tight monolayer of human epithelial cells in vitro. We show that this process is dependent on an initial interaction between alphaLbeta2 integrin CD11a/CD18 on infected monocytic cells and intercellular adhesion molecule 2 (ICAM-2; CD102) and ICAM-3 (CD50) on the apical membrane of epithelial cells.
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