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HIV INFECTIONS

The hidden cost of genetic resistance to HIV-1

Nature Medicine volume 25, pages 878–879 (2019)Cite this article

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This article was retracted on 08 October 2019

This article has been updated

Assessment of more than 400,000 people over the age of 40 demonstrates that homozygosity for a CCR5 variant that prevents HIV-1 infection comes at the cost of increased rates of mortality.

Over the past 6 months, two developments in medical science concerning the C–C motif chemokine receptor 5 (CCR5) gene have garnered mainstream media attention. The first was a birth announcement for twins who, without medical justification, had their CCR5 genes randomly mutated by CRISPR during the in vitro fertilization process1. The second story was the news that the ‘London Patient’ was effectively cured of HIV-1 infection, albeit after allogeneic bone marrow transplantation for Hodgkin’s lymphoma, using stem cells from a donor who was homozygous for the CCR5-Δ32 variant2. Now, with this media frenzy as a backdrop and after years of attempts to develop anti-HIV-1 therapies targeting CCR5, as well as ongoing debate in the literature concerning the consequences of CCR5 loss-of-function mutations, a new study in this issue of Nature Medicine concludes that homozygosity for CCR5-Δ32 comes with an increased rate of mortality3.

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Fig. 1: There is an increased mortality rate among people homozygous for CCR5-Δ32.

Change history

  • 08 October 2019

    An amendment to this paper has been published and can be accessed via a link at the top of the paper.

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Authors and Affiliations

  1. Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA, USA

    Jeremy Luban

  2. Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, MA, USA

    Jeremy Luban

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  1. Jeremy Luban
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Correspondence to Jeremy Luban.

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The author declares no competing interests.

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Luban, J. The hidden cost of genetic resistance to HIV-1. Nat Med 25, 878–879 (2019). https://doi.org/10.1038/s41591-019-0481-8

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