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首页> 外文期刊>Cytokine >Heterozygous defect in HIV-1 coreceptor CCR5 and chemokine production.
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Heterozygous defect in HIV-1 coreceptor CCR5 and chemokine production.

机译：HIV-1受体CCR5和趋化因子产生中的杂合缺陷。

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摘要

CC chemokine receptor 5 (CCR5) is a cell entry cofactor for macrophage-tropic isolates of human immunodeficiency virus 1 (HIV-1). An inactive CCR5 allele with a 32-nucleotide deletion (CCR5Delta32) has been described that confers resistance to HIV-1 infection in homozygotes and slows the rate of progression to AIDS in heterozygotes. We found the allele CCR5Delta32 to be not rare in 399 Swiss blood donors with a frequency of 0.080. To assess the influence of defective CCR5 on production of its ligands we determined the capacity to produce the chemokines macrophage inflammatory protein (MIP)-1alpha, MIP-1beta and RANTES in comparison with the production of the CXC chemokine IL-8 which does not bind to CCR5. Production of chemokines was determined during endotoxin stimulation of whole-blood samples ex vivo. Both, basal and LPS-induced chemokine production in 32 blood donors heterozygous for CCR5Delta32 were not significantly different when compared with 55 blood donors who were homozygous for the wild type CCR5 allele. Copyright 1999 Academic Press.
机译：CC趋化因子受体5（CCR5）是人类免疫缺陷病毒1（HIV-1）巨噬细胞嗜性分离株的细胞进入辅助因子。已经描述了具有32个核苷酸缺失的无活性CCR5等位基因（CCR5Delta32），赋予纯合子以抵抗HIV-1的感染，并减慢了杂合子向AIDS的发展速度。我们发现等位基因CCR5Delta32在399个瑞士献血者中并不罕见，频率为0.080。为了评估有缺陷的CCR5对其配体产生的影响，我们确定了与不结合的CXC趋化因子IL-8的产生相比，产生趋化因子巨噬细胞炎性蛋白（MIP）-1alpha，MIP-1beta和RANTES的能力到CCR5。在离体全血样品的内毒素刺激过程中确定趋化因子的产生。与55个野生型CCR5等位基因纯合子的供血者相比，在32个CCR5Delta32杂合子的供血者中基础和LPS诱导的趋化因子的产生均无显着差异。版权所有1999，学术出版社。

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