Brinkman K, Koopmans P P
Academisch Ziekenhuis, afd. Algemeen Interne Geneeskunde, Nijmegen.
Ned Tijdschr Geneeskd. 1998 Mar 14;142(11):566-72.
Chemokine receptors appear to be essential coreceptors (next to the CD4 receptor) for viral entry of HIV. Non syncytium inducing (NSI) HIV variants (monocytotropic) use the beta-chemokine receptor CCR5, syncytium inducing (SI) variants (lymphocytotropic) the alpha-chemokine receptor CXCR4. Mutations in CCR5 appear to give protection against HIV infection and to slow disease progression. Blocking of chemokine receptors interrupts HIV infection in vitro and offers new options for therapeutic strategies. Theoretical progress has been made in the development of an animal model for HIV infection owing to the elucidation of the role of chemokine receptors in HIV entry into the cell. In the future HIV variants will be classified according to their interaction with chemokine receptors.
趋化因子受体似乎是HIV病毒进入细胞的重要共受体(仅次于CD4受体)。非合胞体诱导型(NSI)HIV变异株(嗜单核细胞型)利用β趋化因子受体CCR5,合胞体诱导型(SI)变异株(嗜淋巴细胞型)利用α趋化因子受体CXCR4。CCR5突变似乎能预防HIV感染并减缓疾病进展。阻断趋化因子受体可在体外阻断HIV感染,并为治疗策略提供新选择。由于阐明了趋化因子受体在HIV进入细胞中的作用,在HIV感染动物模型的开发方面取得了理论进展。未来,HIV变异株将根据它们与趋化因子受体的相互作用进行分类。