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Monday, October 03, 2005 

Black plague, AIDS, and nursery rhymes over on DailyKos

DarkSyde on DailyKos discusses an appropriate October topic: Night of the Living Dead: Blood Warriors. After giving a history of the 14th century bubonic plague outbreak (complete with pictures of modern plague victims!), he discusses the possible link between that episode and the genetics of resistance to HIV. However, I have a quibble. It's not been shown definitively that Yersinia pestis, the bacterium which causes plague, was actually the pressure that caused a selection for the CCR5 delta 32 allele.

Continued on the flip side...

A few articles on the CCR5/plague connection:

Genes Immun. 2005 Apr 7

Detection of the CCR5-Delta32 HIV resistance gene in Bronze Age skeletons.

Hummel S, Schmidt D, Kremeyer B, Herrmann B, Oppermann M.

A mutant allele of the chemokine receptor CCR5 gene (CCR5-Delta32), which confers resistance to HIV-1 infection, is believed to have originated from a single mutation event in historic times, and rapidly expanded in Caucasian populations, owing to an unknown selective advantage. Among other candidates, the plague bacillus Yersinia pestis was implicated as a potential source of strong selective pressure on European populations during medieval times. Here, we report amplifications of the CCR5-Delta32 DNA sequence from up to 2900-year-old skeletal remains from different burial sites in central Germany and southern Italy. Furthermore, the allele frequency of CCR5-Delta32 in victims of the 14th century plague pandemic in Lubeck/northern Germany was not different from a historic control group. Our findings indicate that this mutation was prevalent already among prehistoric Europeans. The results also argue against the possibility of plague representing a major selective force that caused rapid increase in CCR5-Delta32 gene frequencies within these populations.


Nature. 2004 Feb 12;427(6975):606.

Evolutionary genetics: CCR5 mutation and plague protection.

Mecsas J, Franklin G, Kuziel WA, Brubaker RR, Falkow S, Mosier DE.

A recent and prevalent mutation in the chemokine receptor CCR5 in humans of northern European ancestry has been proposed to provide protection against bubonic plague. 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 Ages, 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.


and a comment on that article:

Nature. 2004 Jul 22;430(6998):417

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

Elvin SJ, Williamson ED, Scott JC, Smith JN, Perez De Lema G, Chilla S, Clapham P, Pfeffer K, Schlondorff D, Luckow B.

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.


Smallpox has been suggested as a possible reason instead of plague:

Proc Natl Acad Sci U S A. 2003 Dec 9;100(25):15276-9.

Evaluating plague and smallpox as historical selective pressures for the CCR5-Delta 32 HIV-resistance allele.

Galvani AP, Slatkin M.

The high frequency, recent origin, and geographic distribution of the CCR5-Delta 32 deletion allele together indicate that it has been intensely selected in Europe. Although the allele confers resistance against HIV-1, HIV has not existed in the human population long enough to account for this selective pressure. The prevailing hypothesis is that the selective rise of CCR5-Delta 32 to its current frequency can be attributed to bubonic plague. By using a population genetic framework that takes into account the temporal pattern and age-dependent nature of specific diseases, we find that smallpox is more consistent with this historical role.


All in all, a very good article...I just don't feel it's correct to say confidently that plague caused the spread of the CCR5 delta 32 allele.

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  • I'm Tara C. Smith
  • From Iowa, United States
  • I'm a mom and a scientist, your basic stressed-out, wanna-have-it-all-and-do-it-all Gen Xer. Recently transplanted from Ohio to Iowa, I've spent most of my life in the midwest (with 4 years of college spent out east in "soda" territory). My main interest, and the subject of my research, is infectious disease: how does the microbe cause illness? What makes one strain nasty, and another "avirulent?" Are the latter really not causing any disease, or could some of those be possible for the development of chronic disease years down the road? Additionally, I've spent a lot of time discussing the value of teaching evolution, and educating others about "intelligent design" and other forms of creationism. My interest in history of science and medicine is also useful as a way to tie all of the above interests together. [Disclaimer: the views here are solely my own, and do not represent my employer, my spouse, that guy who's always sitting by the fountain when I come into work, or anyone else with whom I may be remotely affiliated.]
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