CCR5 mutation and plague protection

Joan Mecsas, Greg Franklin, William A. Kuziel, Robert R. Brubaker, Stanley Falkow and Donald E. Mosier ()
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Joan Mecsas: Stanford University School of Medicine
Greg Franklin: The Scripps Research Institute
William A. Kuziel: Section of Molecular Genetics and Microbiology and Institute of Cellular and Molecular Biology, University of Texas at Austin
Robert R. Brubaker: Michigan State University
Stanley Falkow: Stanford University School of Medicine
Donald E. Mosier: The Scripps Research Institute

Nature, 2004, vol. 427, issue 6975, 606-606

Abstract: Abstract A recent and prevalent mutation in the chemokine receptor CCR5 in humans of northern European ancestry has been proposed to provide protection against bubonic plague1,2. Here we infect both normal and CCR5-deficient mice with the bacterium Yersinia pestis, the cause of the plague epidemics that wiped out one-third of Europeans in the Middle Ages3, and find no difference in either bacterial growth or survival time between the two groups. Unless the pathogenesis of Yersinia infection differs markedly between mice and humans, our results indicate that CCR5 deficiency in people is unlikely to protect against plague.

Date: 2004
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DOI: 10.1038/427606a

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