Department of Basic Sciences, California Northstate University College of Medicine, Elk Grove, California, USA.
J Infect Dis. 2023 Jul 14;228(2):116-121. doi: 10.1093/infdis/jiad062.
We analyzed findings in a same-gender couple discordant in their human immunodeficiency virus (HIV) status. The HIV+ partner was homozygous for CCR5 while his receptive HIV- partner was a CCR5Δ32 heterozygote with a C20S missense mutation in his CCR5 allele. The cells from the HIV- partner showed significant resistance to R5 fusion/infection and had no chemotactic response to CCL4 (macrophage inflammatory protein 1β). We demonstrated abundant CCR5-specific RNA in the HIV- partner's cells but no detectable CCR5 protein. CCR5 promoter region cloned from each partner's DNA indicated no significant impact on RNA transcription. The compound effect of CCR5Δ32 and C20S mutation impaired CCR5 coreceptor function and conferred resistance to HIV-1.
我们分析了一对人类免疫缺陷病毒（HIV）状况不一致的同性伴侣的研究结果。HIV+ 伴侣是 CCR5 纯合子，而他的 HIV- 接受者是 CCR5Δ32 杂合子，其 CCR5 等位基因中有 C20S 错义突变。来自 HIV- 伴侣的细胞对 R5 融合/感染表现出显著的抗性，并且对 CCL4（巨噬细胞炎症蛋白 1β）没有趋化反应。我们在 HIV- 伴侣的细胞中检测到大量的 CCR5 特异性 RNA，但未检测到 CCR5 蛋白。从每个伴侣的 DNA 中克隆的 CCR5 启动子区域表明对 RNA 转录没有显著影响。CCR5Δ32 和 C20S 突变的复合效应削弱了 CCR5 辅助受体功能，并赋予对 HIV-1 的抗性。
