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Evolutionary genetics: Ambiguous role of CCR5 in Y. pestis infection.

Abstract
Mecsas and colleagues suggest that a deficiency in the chemokine receptor CCR5 in humans is unlikely to confer protection against plague, based on their study of Yersinia pestis infection in Ccr5-deficient mice. They were testing the hypothesis that a mutation in the CCR5 gene, frequently found in Caucasians, may have been selected for in the past because it provided protection against (bubonic) plague; the mutation, called CCR5Delta32, is characterized by a 32-base-pair deletion. We have also tested this hypothesis by using Y. pestis infection in mice and, in addition, we have done phagocytosis experiments with macrophages from wild-type and Ccr5-deficient mice. Although, like Mecsas et al., we did not see any difference in the survival of the two groups of mice, we did find that there was a significantly reduced uptake of Y. pestis by Ccr5-deficient macrophages in vitro. Our results indicate that the role of Ccr5 in Y. pestis infection may therefore be more complex than previously thought.
AuthorsStephen J Elvin, E Diane Williamson, Joanne C Scott, Jeremy N Smith, Guillermo Pérez De Lema, Silvia Chilla, Paul Clapham, Klaus Pfeffer, Detlef Schlöndorff, Bruno Luckow
JournalNature (Nature) Vol. 430 Issue 6998 Pg. 417 (Jul 22 2004) ISSN: 1476-4687 [Electronic] England
PMID15272490 (Publication Type: Journal Article, Comment)
Chemical References
  • Receptors, CCR5
Topics
  • Animals
  • Evolution, Molecular
  • Humans
  • Macrophages (cytology, immunology, metabolism, microbiology)
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Models, Biological
  • Phagocytosis
  • Plague (genetics, metabolism, microbiology)
  • Receptors, CCR5 (deficiency, genetics, metabolism)
  • Sequence Deletion (genetics)
  • Survival Rate
  • Virulence
  • White People (genetics)
  • Yersinia pestis (pathogenicity, physiology)

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