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Evolutionary genetics: CCR5 mutation and plague protection.

Joan Mecsas¹, Greg Franklin, William A Kuziel

¹Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California 94305-5402, USA.

|February 13, 2004

Summary

CCR5 deficiency may not protect against bubonic plague. Researchers infected normal and CCR5-deficient mice with Yersinia pestis, finding no difference in outcomes, suggesting the mutation offers no protection against this deadly bacterium.

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Area of Science:

Immunology
Genetics
Infectious Diseases
Evolutionary Medicine

Background:

A prevalent CCR5 (chemokine receptor type 5) mutation in Northern European populations has been hypothesized to confer protection against Yersinia pestis, the bacterium responsible for bubonic plague.
The historical impact of plague epidemics, particularly the one in the Middle Ages, highlights the significant public health implications of understanding host-pathogen interactions and potential genetic resistance factors.

Purpose of the Study:

To investigate the role of CCR5 deficiency in susceptibility and resistance to Yersinia pestis infection.
To experimentally test the proposed protective effect of the CCR5 mutation against bubonic plague.

Main Methods:

Infection of genetically modified mice lacking functional CCR5 receptors with Yersinia pestis.
Comparison of bacterial growth kinetics and survival rates between CCR5-deficient and normal (wild-type) mice.
Utilizing a murine model to simulate Yersinia pestis infection relevant to bubonic plague.

Main Results:

No significant difference was observed in bacterial growth of Yersinia pestis between normal mice and CCR5-deficient mice.
Survival times following Yersinia pestis infection were comparable in both experimental groups (normal vs. CCR5-deficient mice).
The CCR5 deficiency did not confer any discernible advantage or protection against the lethal effects of the bacterium in the studied model.

Conclusions:

The findings suggest that CCR5 deficiency is unlikely to be the protective factor against bubonic plague in humans.
The study indicates that the proposed link between CCR5 mutation and plague resistance may not be valid, unless Yersinia pestis pathogenesis differs significantly between mice and humans.
Further research is warranted to explore other potential genetic or environmental factors influencing human resistance to Yersinia pestis.