Malo A, Rommel F, Bogner J, Gruber R, Schramm W, Goebel F D, Riethmüller G, Wank R
Institut für Immunologie, Universität München, Germany.
Immunobiology. 1998 Feb;198(4):485-8. doi: 10.1016/S0171-2985(98)80055-7.
The CCR5 chemokine receptor is an important coreceptor for macrophage-tropic HIV strains. Homozygous carriers of the mutated CCR5 receptor with a 32 bp deletion (delta 32-CCR5) are highly protected against HIV infection. A protective effect has also been described for heterozygous individuals carrying both mutated and wildtype CCR5 receptors. We compared the frequency of the mutated delta 32-CCR5 HIV coreceptor in HIV positive patients infected by sexual contact (N = 160) with intravenously HIV infected hemophilic patients (N = 84) and HIV negative individuals (N = 421). We found no protective effect of delta 32-CCR5 HIV coreceptor in hemophilic patients (p = 0.0134). If proteins of plasma concentrates would be responsible for facilitating the entry of HIV macrophages by upregulation of the CCR5 wildtype receptor it would be of therapeutical interest to identify the responsible plasma proteins.
CCR5趋化因子受体是嗜巨噬细胞性HIV毒株的重要共受体。携带32bp缺失的突变CCR5受体（δ32-CCR5）的纯合子携带者对HIV感染具有高度抵抗力。对于同时携带突变型和野生型CCR5受体的杂合个体，也有保护作用的描述。我们比较了通过性接触感染HIV的患者（N = 160）、静脉注射感染HIV的血友病患者（N = 84）和HIV阴性个体（N = 421）中突变型δ32-CCR5 HIV共受体的频率。我们发现δ32-CCR5 HIV共受体在血友病患者中没有保护作用（p = 0.0134）。如果血浆浓缩物中的蛋白质通过上调CCR5野生型受体促进HIV巨噬细胞的进入，那么鉴定出相关的血浆蛋白质将具有治疗意义。
