HLA and other host factors in transfusion-acquired HIV-1 infection
HLA and other host factors in transfusion-acquired HIV-1 infection
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DOI：
10.1016/s0198-8859(99)00142-1
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发表时间：
2000-02-01
期刊：
影响因子：
2.7
通讯作者：
Sullivan, JS
中科院分区：
文献类型：
--
作者：
Geczy, AF;Kuipers, H;Sullivan, JS
感染HIV-1的宿主和病毒因素差异很大，有些人在感染后3至5年内进展为艾滋病，而另一些人在临床上仍无症状长达10年以上。可能导致疾病进展的宿主因素包括人类白细胞抗原和趋化因子受体CCR5和CCR2的等位基因变体，这些因素已被证明影响长期生存和快速进展。在这项研究中，我们研究了HT-A以及CCR5和CCR2基因的多态性对输血获得性HIV-1感染患者长期生存的贡献。我们发现，与HIV-1阴性的澳大利亚高加索人群相比，研究组中的HLA-A32和-A25等位基因数量较多，而HLA-B8等位基因的数量较少。然而，CCR5和CCR2的等位基因变异对长期生存没有明显的贡献，而且在这个相对较小的研究对象组(n=20)中，无法评估HLA和CCR基因多态的联合影响。这项工作的结果支持人类白细胞抗原在长期无进展中的作用，尽管在悉尼血库队列中存在新缺陷的艾滋病毒-1 MAP混淆了某些人类白细胞抗原等位基因与面对艾滋病毒-1感染的长期生存之间的关联。《人类免疫学》61,172-176(2000)。(C)美国组织相容性和免疫遗传学会，2000年。爱思唯尔科学公司出版。
The host and viral factors that underlie infection with HIV-1 vary considerably with some individuals progressing to AIDS within 3 to 5 years after infection, whereas others remain clinically asymptomatic for over 10 years. Host factors thar may contribute to disease progression include HLA and allelic variants of the chemokine receptors CCR5 and CCR2, which have been shown to influence both long-term survival and rapid progression. In this study, we have examined the contribution of HT-A and polymorphisms in CCR5 and CCR2 to long-term survival in transfusion-acquired HIV-1-infrcted individuals. We have found a higher number of HLA-A32 and -A25 alleles bur a lower number of the HLA-B8 allele in the study group compared with the frequencies seen in the HIV-1-negative Australian caucasian population. However, there was no apparent contribution by allelic variants of CCR5 and CCR2 to long-term survival and the combined influence of HLA and CCR polymorphisms could not be evaluated in this relatively small (n = 20) group of study subjects. The results of this work support a role for HLA in long-term nonprogression though the presence in the Sydney Blood Lank Cohort of nef-defective HIV-1 map confound associations between certain HLA alleles and long-term survival in the face of infection with HIV-1. Human Immunology 61, 172-176 (2000). (C) American Society for Histocompatibility and Immunogenetics, 2000. Published by Elsevier Science Inc.