Genotypes at chromosome 22q12-13 are associated with HIV-1-exposed but uninfected status in Italians

Genotypes at chromosome 22q12-13 are associated with HIV-1-exposed but uninfected status in Italians
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DOI:
10.1097/01.aids.0000174447.48003.dd
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发表时间:
2005-07-01
期刊:
影响因子:
3.8
通讯作者:
Miyazawa, M
Miyazawa, M
中科院分区:
医学2区
文献类型:
--
作者:
Kanari, Y;Clerici, M;Miyazawa, M

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目的:尽管多次和反复暴露于HIV-1,但有些人没有可检测到的HIV基因组,并显示出对病毒抗原的T细胞记忆反应。在这些未感染的个体中检测到HIV-1反应性粘膜伊加表明他们可能对HIV具有免疫抵抗力。我们测试了上述HIV-1暴露但未感染的状态是否与CCR 5基因纯合缺失以外的遗传标记相关。基于我们在小鼠逆转录病毒感染中控制中和抗体产生的基因的15号染色体上的定位,我们对42名暴露于HIV-1但未感染的意大利人在人类22号染色体同线片段的多态性位点进行了基因分型,结果:在HIV-1感染者中,染色体22 q12 -13基因型与一个可能的显性位点有显著的相关性。22号染色体上的连锁不平衡分布也不同的暴露,但未感染和其他两个表型groups.Conclusions:数据表明存在一个新的遗传因素与HIV-1暴露,但未感染的状态。(c)2005年利平科特威廉姆斯&威尔金斯。
Objective: Despite multiple and repeated exposures to HIV-1, some individuals possess no detectable HIV genome and show T-cell memory responses to the viral antigens. HIV-1-reactive mucosal IgA detected in such uninfected individuals suggests their possible immune resistance against HIV. We tested if the above HIV-1-exposed but uninfected status was associated with genetic markers other than a homozygous deletion of the CCR5 gene.Methods: Based on our mapping in chromosome 15 of a gene controlling the production of neutralizing antibodies in a mouse retrovirus infection, we genotyped 42 HIV-1-exposed but uninfected Italians at polymorphic loci in the syntenic segment of human chromosome 22, and compared them with 49 HIV-1-infected and 47 uninfected healthy control individuals by a closed testing procedure.Results: A significant association was found between chromosome 22q12-13 genotypes and a putative dominant locus conferring anti-HIV-1 immune responses in the exposed but uninfected individuals. Distributions of linkage disequilibrium across chromosome 22 also differed between the exposed but uninfected and two other phenotypic groups.Conclusions: The data indicated the presence of a new genetic factor associated with the HIV-1-exposed but uninfected status. (c) 2005 Lippincott Williams & Wilkins.