C–C chemokine receptor (CCR) 5 (CCR5) is the main HIV-1 coreceptor involved in virus entry and cell-to-cell spread during acute and chronic infections: such CCR5 and T cell tropic viruses are adapted to and replicate in CD4⁺ memory T cells. Polymorphisms in CCR5 regulate CCR5 expression, which, in turn, influences HIV infection acquisition and subsequent disease progression. Among these polymorphisms, a 32-bp deletion in the CCR5 open reading frame (CCR5 Δ32) and a single nucleotide polymorphism (SNP) in the promoter (−2459G/A) are the most well-characterized polymorphisms. CCR5 Δ32 provides partial to full protection against HIV infection and, therefore, serves as a basis for gene deletion studies attempting to achieve a permanent HIV cure. Recent studies have discovered that certain SNPs in the CCR region, not within CCR5, also affect CCR5 expression, HIV infection, and disease progression. Although these studies provide further valuable information regarding the role of human genetic variation in HIV/AIDS, they did not incorporate −2459G/A. In this article, the author summarizes the knowledge gained through the discovery of these new SNPs and introduces the idea that by not incorporating −2459G/A, less comprehensive conclusions may have been reached. Until a strategy that delivers a cure to the millions is found, every piece of information that may help curtail the HIV/AIDS threat to public health should be considered useful.

中文翻译：

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关于 CCR5、HIV 感染和疾病进展的新知识：“旧”还有价值吗？

C-C 趋化因子受体 (CCR) 5 (CCR5) 是主要的 HIV-1 辅助受体，在急性和慢性感染期间参与病毒进入和细胞间传播：此类 CCR5 和 T 细胞嗜性病毒适应 CD4 并在 CD4 中复制⁺记忆 T 细胞。CCR5中的多态性调节 CCR5 表达，进而影响 HIV 感染的获得和随后的疾病进展。在这些多态性中，CCR5开放阅读框 ( CCR5 Δ32) 中的 32-bp 缺失和启动子 (-2459G/A) 中的单核苷酸多态性 (SNP) 是最充分表征的多态性。CCR5Δ32 对 HIV 感染提供部分或全面的保护，因此，作为基因缺失研究的基础，试图实现 HIV 的永久性治愈。最近的研究发现，某些 SNP 在CCR区域内，而不是在CCR5内，也影响 CCR5 表达、HIV 感染和疾病进展。尽管这些研究提供了有关人类遗传变异在 HIV/AIDS 中的作用的进一步有价值的信息，但它们并未纳入 -2459G/A。在这篇文章中，作者总结了通过发现这些新的 SNP 获得的知识，并介绍了不包含 -2459G/A 的想法，可能会得出不太全面的结论。在找到可以治愈数百万人的策略之前，每一条可能有助于减少 HIV/AIDS 对公共健康的威胁的信息都应该被认为是有用的。