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Reported CCR5-∆32 deviation from Hardy-Weinberg equilibrium is explained by poor genotyping of rs62625034

View ORCID ProfileYosuke Tanigawa, View ORCID ProfileManuel A. Rivas
doi: https://doi.org/10.1101/791517
Yosuke Tanigawa
1Department of Biomedical Data Science, Stanford University, Stanford, CA, 94305
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Manuel A. Rivas
1Department of Biomedical Data Science, Stanford University, Stanford, CA, 94305
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  • For correspondence: mrivas@stanford.edu
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Abstract

In the fall of 2018, news broke about a researcher from China who had used CRISPR gene editing to cause human babies to have a deletion in the CCR5 chemokine receptor, making them resistant to HIV infection. One of the numerous ethical concerns about this study is that the deletion may have other effects. Subsequently, Nature Medicine published a Brief Communications from Wei and Nielsen concluding that homozygotes for the CCR5-∆32 deletion have a survival probability to age 76 of 83.5% compared to 86.5% and 86.4% for the heterozygotes and the other homozygote, respectively, and that observed departures from Hardy Weinberg proportions also support selection operating on this allele1. In the study, Wei and Nielsen used a proxy variant, rs62625034 in their analysis. Here, we report that the reported CCR5-∆32 deviation from Hardy-Weinberg equilibrium (HWE) inferred by Wei and Nielsen can be explained by poor genotyping of rs62625034, the variant used for their analysis.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license.
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Posted October 14, 2019.
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Reported CCR5-∆32 deviation from Hardy-Weinberg equilibrium is explained by poor genotyping of rs62625034
Yosuke Tanigawa, Manuel A. Rivas
bioRxiv 791517; doi: https://doi.org/10.1101/791517
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Reported CCR5-∆32 deviation from Hardy-Weinberg equilibrium is explained by poor genotyping of rs62625034
Yosuke Tanigawa, Manuel A. Rivas
bioRxiv 791517; doi: https://doi.org/10.1101/791517

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