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首页> 外文期刊>AIDS Research and Human Retroviruses >Association of human mannose receptor in sexual transmission of human immunodeficiency virus in serodiscordant couples
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Association of human mannose receptor in sexual transmission of human immunodeficiency virus in serodiscordant couples

机译：人类甘露糖受体与血清黏附剂对人类免疫缺陷病毒性传播的关系

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HIV binds specifically to the human mannose receptor (hMR) on vaginal epithelial cells that are devoid of a conventional CD4 receptor. HIV binding to hMR on vaginal epithelial cells induces the production of matrix metalloproteinase 9 (MMP9) leading to degradation of the extracellular matrix, which may increase the risk of HIV entry into vaginal epithelial cells and further transmission into distal cells. Immunofluorescent localization of hMR on vaginal epithelial cells of seronegative females from the general population included the control group (n=52) and seronegative females from serodiscordant couples. There was PCR amplification of DNA from peripheral blood mononuclear cells (PBMCs) of the serodiscordant females for the CCR5 gene flanking the CCR5-Δ32 region; PCR amplification and sequencing of the C2-V3 region of HIV variants in PBMCs and sperm of the infected male partners of the serodiscordant couples; and the presence of hMR on 0-11% of the vaginal epithelial cells of seronegative females (n=39) from serodiscordant couples and 90-95% that of a control group of females (n=52). Nine of these serodiscordant females did not show a CCR5-Δ32 deletion. The translated amino acid sequence of the C2-V3 region of the env gene of HIV-1C in PBMCs (n=9) and sperm (n=5) of the male partners showed the presence of distinct variants and the variation in PBMCs and sperm of serodiscordant males was almost similar to that of infected males from concordant couples. The presence of hMR in a smaller number of vaginal epithelial cells of serodiscordant females prevented binding and HIV entry into these cells and therefore prevented sexual transmission of HIV.
机译：HIV与缺乏常规CD4受体的阴道上皮细胞上的人甘露糖受体（hMR）特异性结合。 HIV与阴道上皮细胞上的hMR结合会诱导基质金属蛋白酶9（MMP9）的产生，导致细胞外基质降解，这可能会增加HIV进入阴道上皮细胞并进一步传播至远端细胞的风险。 hMR在普通人群血清阴性女性阴道上皮细胞上的免疫荧光定位包括对照组（n = 52）和血清抗体异常女性血清阴性。 PCR扩增来自血清抗体的女性外周血单核细胞（PBMC）的DNA，用于CCR5-Δ32区域两侧的CCR5基因。 PBMC和血清抗体的夫妇的被感染男性伴侣精子中HIV变异的C2-V3区的PCR扩增和测序;血清反应阴性夫妇的血清阴性女性（n = 39）的阴道上皮细胞（n = 39）的0-11％和对照组女性（n = 52）的90-95％的hMR的存在。这些血清抗体的女性中有9位未显示CCR5-Δ32缺失。男性伴侣的PBMC（n = 9）和精子（n = 5）中HIV-1C env基因C2-V3区的翻译的氨基酸序列显示存在明显的变异以及PBMC和精子的变异Serodiscordant男性的感染率几乎与一致配偶的感染男性相似。 hMR的存在使血清胶粘剂的女性的阴道上皮细胞数量减少，从而阻止了结合以及HIV进入这些细胞，从而阻止了HIV的性传播。

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