Homozygous Delta 32 deletion of the CCR-5 chemokine receptor gene in an HIV-1-infected patient
Homozygous Delta 32 deletion of the CCR-5 chemokine receptor gene in an HIV-1-infected patient
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DOI：
10.1097/00002030-199710000-00001
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发表时间：
1997-08-01
期刊：
影响因子：
3.8
通讯作者：
Galli, M
中科院分区：
文献类型：
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作者：
Balotta, C;Bagnarelli, P;Galli, M
背景：最近的研究发现，非合胞诱导（NSI）、嗜单核巨噬细胞的HIV-1分离株的进入需要结合CD4和CCR5受体，并且Delta 32/Delta 32纯合子个体可以保护其免受感染。目的：分析hiv -1感染者和未感染者CCR-5基因多态性。设计与方法：采用聚合酶链反应（PCR）从外周血单个核细胞DNA中扩增CCR-5序列。对152例hiv - 1感染者和122例未感染对照进行了32个碱基对缺失的检测。通过病毒分离和MT-2评价确定HIV-1表型。结果：野生型/Delta 32杂合子和Delta 32/Delta 32纯合子分别在健康对照组的10.7和0.8%以及hiv -1感染者的9.8和0.7%中存在。值得注意的是，通过PCR检测到CCR-5基因的Delta 32/Delta 32缺失，并在具有SI表型的进行性感染的B进化支病毒患者中测序证实。结论：CCR-5基因的Delta 32/Delta 32纯合性并不能绝对保护HIV-1感染，这表明嗜巨噬病毒毒株可以使用CCR-5以外的辅助受体，也可以独立于功能性CCR-5辅助受体的存在而感染HIV-1。另外，嗜t细胞分离株持续的原发感染，虽然例外，也可能发生。
Background: Recent research has found that entry of non-syncytium-inducing (NSI), monocyte-macrophage-tropic HIV-1 isolates requires binding to both CD4 and CCR5 receptors, and that Delta 32/Delta 32 homozygous individuals are protected against infection.Objective: To analyse the polymorphism of CCR-5 gene in HIV-1-infected and uninfected subjects.Design and methods: CCR-5 sequences were amplified by polymerase chain reaction (PCR) from DNA of peripheral blood mononuclear cells. Samples from 152 HIV-l-infected subjects and 122 uninfected controls were tested for the detection of the 32 base-pair deletion. HIV-1 phenotype was determined by viral isolation and MT-2 evaluation.Results: The wild-type/Delta 32 heterozygous and Delta 32/Delta 32 homozygous conditions were represented in 10.7 and 0.8% of healthy controls and in 9.8 and 0.7% of HIV-1-infected subjects, respectively. Of note, the Delta 32/Delta 32 deletion of the CCR-5 gene was detected by PCR and sequencing confirmed in a patient with progressive infection harbouring a clade B virus with SI phenotype.Conclusions: Delta 32/Delta 32 homozygosity for the CCR-5 gene does not confer absolute protection against HIV-1 infection, suggesting that either macrophage-tropic viral strains could use coreceptors other than CCR-5 or infect independently of the presence of a functional CCR-5 coreceptor. Alternatively, primary infection sustained by T-cell-tropic isolates, although exceptional, may occur.