Smoleń-Dzirba Joanna, Rosińska Magdalena, Janiec Janusz, Beniowski Marek, Cycoń Mariusz, Bratosiewicz-Wąsik Jolanta, Wąsik Tomasz J
Department of Microbiology and Virology, School of Pharmacy with the Division of Laboratory Medicine in Sosnowiec, Medical University of Silesia, Katowice, Poland.
Department of Epidemiology, National Institute of Public Health - National Institute of Hygiene, Warsaw, Poland.
AIDS Rev. 2017 Dec;19(4):219-230.
CC-chemokine receptor 5 serves as the coreceptor for the HIV-1 R5 strains, which are responsible for the majority of HIV transmissions. A deletion of 32 nucleotides in the gene encoding this receptor (termed CCR5-Δ32) leads to the suppression of CC-chemokine receptor 5 presentation at the cell surface, thus impeding process of HIV entry into the cell. Individuals homozygous for the CCR5-Δ32 allele are resistant to infection with HIV-1 R5 strains, and are extremely rare among HIV-1-infected individuals. We have described a case of person homozygous for CCR5-Δ32, who was infected with subtype B HIV-1. Based on examination of proviral V3 sequences obtained from the first clinical blood sample within less than five months after seroconversion, the CXC-chemokine receptor 4-using strains (X4 or R5/X4) were detected. Data on HIV-1-infected patients homozygous for the CCR5-Δ32 allele, course of HIV-1 infection in these cases, and the infecting viral strains from current and all former reports on HIV-1 infection in CCR5-Δ32 homozygotes were gathered and compared. Identification of HIV-1-infected persons homozygous for CCR5-Δ32 supports the evidence that the lack of functional CC-chemokine receptor 5 at the cell surface does not confer absolute protection against HIV-1 infection, which should be considered when designing future HIV pre-exposure prophylaxis schemes basing on CC-chemokine receptor 5 blocking drugs.
CC趋化因子受体5作为HIV-1 R5毒株的共受体，而这些毒株导致了大多数的HIV传播。编码该受体的基因中32个核苷酸的缺失（称为CCR5-Δ32）会导致CC趋化因子受体5在细胞表面的表达受到抑制，从而阻碍HIV进入细胞的过程。CCR5-Δ32等位基因纯合的个体对HIV-1 R5毒株感染具有抗性，并且在HIV-1感染个体中极为罕见。我们描述了一例CCR5-Δ32纯合的个体，其感染了B亚型HIV-1。基于对血清转化后不到五个月内从首次临床血样中获得的前病毒V3序列的检测，发现了使用CXC趋化因子受体4的毒株（X4或R5/X4）。收集并比较了关于CCR5-Δ32等位基因纯合的HIV-1感染患者的数据、这些病例中HIV-1感染的病程以及来自目前和所有既往关于CCR5-Δ32纯合子中HIV-1感染报告的感染病毒株。鉴定出CCR5-Δ32纯合的HIV-1感染个体支持了以下证据：细胞表面缺乏功能性CC趋化因子受体5并不能提供针对HIV-1感染的绝对保护，在设计未来基于CC趋化因子受体5阻断药物的HIV暴露前预防方案时应考虑这一点。
