首页> 外文期刊>The Journal of Infectious Diseases >Epidemiologic and biologic characterization of a cohort of human immunodeficiency virus type 1 highly exposed, persistently seronegative female sex workers in northern Thailand. Chiang Mai HEPS Working Group.
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Epidemiologic and biologic characterization of a cohort of human immunodeficiency virus type 1 highly exposed, persistently seronegative female sex workers in northern Thailand. Chiang Mai HEPS Working Group.

机译:在泰国北部,一组高度暴露,持续血清阴性的女性性工作者的人类免疫缺陷病毒1型队列的流行病学和生物学特征。清迈HEPS工作组。

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摘要

Characterization of persons highly exposed to human immunodeficiency virus (HIV)-1 who remain uninfected may help define protective immunity. Seventeen HIV-1-seronegative Thai female sex workers (CSWs) with epidemiologic evidence of exposure to HIV-1 were studied for humoral immune responses and phenotypic and genotypic analyses of HLA class I and CCR5 allelic profiles. Infected CSWs and low-risk HIV-1-seronegative Thai women were controls. Highly exposed, persistently seronegative (HEPS) CSWs did not differ from HIV-infected CSWs in HIV risks, condom use, or sexually transmitted diseases. Significant differences were seen in humoral immune responses: gp160-specific IgA responses were detected in cervicovaginal lavage fluids in 6 of 13 HEPS CSWs but 0 of 21 seronegative subjects. All women had wild-type CCR5. HEPS CSWs were more likely to have the HLA-B18 phenotype and genotype than were matched controls (corrected P=.018). Epidemiologic exposure to HIV-1 without apparent infection, an unusual distribution of HLA class I alleles, and HIV-1 gp160-specific IgA responses suggest a biologic basis for this phenomenon.
机译:高度暴露于未感染的人类免疫缺陷病毒(HIV)-1的人群的特征可能有助于定义保护性免疫。研究了17名具有HIV-1血清反应阴性的泰国女性性工作者(CSW),他们具有暴露于HIV-1的流行病学证据,以进行体液免疫反应以及HLA I类和CCR5等位基因特征的表型和基因型分析。感染的CSW和低风险的HIV-1血清阴性泰国妇女为对照。高度暴露,持续血清阴性(HEPS)的CSW与HIV感染的CSW在HIV风险,使用避孕套或性传播疾病方面没有区别。在体液免疫反应中观察到显着差异:在13例HEPS CSW中有6例在宫颈阴道灌洗液中检测到gp160特异性IgA反应,而在21例血清阴性的受试者中有0例检测到gp160特异性IgA反应。所有妇女均具有野生型CCR5。与匹配的对照相比,HEPS CSWs更可能具有HLA-B18表型和基因型(校正后的P = .018)。没有明显感染的HIV-1流行病学暴露,HLA I类等位基因的异常分布以及HIV-1 gp160特异性IgA反应提示了这种现象的生物学基础。

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