Plague in humans ‘twice as old’ but didn’t begin as flea-borne, ancient DNA reveals

Oct 28, 2015

Credit: Natalia Shishlina

Source: University of Cambridge

New research using ancient DNA has revealed that plague has been endemic in human populations for more than twice as long as previously thought, and that the ancestral plague would have been predominantly spread by human-to-human contact — until genetic mutations allowed Yersinia pestis (Y. pestis), the bacteria that causes plague, to survive in the gut of fleas.

These mutations, which may have occurred near the turn of the 1st millennium BC, gave rise to the bubonic form of plague that spreads at terrifying speed through flea — and consequently rat — carriers. The bubonic plague caused the pandemics that decimated global populations, including the Black Death, which wiped out half the population of Europe in the 14th century.

Before its flea-borne evolution, however, researchers say that plague was in fact endemic in the human populations of Eurasia at least 3,000 years before the first plague pandemic in historical records (the Plague of Justinian in 541 AD).

They say the new evidence that Y. pestis bacterial infection in humans actually emerged around the beginning of the Bronze Age suggests that plague may have been responsible for major population declines believed to have occurred in the late 4th and early 3rd millennium BC.

The work was conducted by an international team including researchers from the universities of Copenhagen, Denmark, and Cambridge, UK, and the findings are published today in the journal Cell.

“We found that the Y. pestis lineage originated and was widespread much earlier than previously thought, and we narrowed the time window as to when and how it developed,” said senior author Professor Eske Willerslev, who recently joined Cambridge University’s Department of Zoology from the University of Copenhagen.

“The underlying mechanisms that facilitated the evolution of Y. pestis are present even today. Learning from the past may help us understand how future pathogens may arise and evolve,” he said.


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10 comments on “Plague in humans ‘twice as old’ but didn’t begin as flea-borne, ancient DNA reveals

  • From the OP:

    These mutations, which may have occurred near the turn of the 1st millennium BC, gave rise to the bubonic form of plague that spreads at terrifying speed through flea — and consequently rat — carriers. The bubonic plague caused the pandemics that decimated global populations, including the Black Death, which wiped out half the population of Europe in the 14th century.

    …wiped out half the population of Europe.. That is some seriously harsh selective pressure!

    So Y pestis spread more effectively through fleas than through the victims coughing? Hmm. Thinking about this. Instead of jumping directly from victim to victim instead it employs an intermediary to transfer. Doesn’t seem so efficient but I must be missing something.



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  • Would that coincide with the increase in population density? Fleas on the back pests would be pretty effective in flea and rat-infested cities. Direct human contact would as well I suppose. Maybe the bacteria isn’t that resilient when airborne.



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  • Missing something:

    Growing intercontinental trade, overland silk routes, maritime activity (rats in ships’ bellies), silks and cloth, bearing fleas, widely traded for millennia, urbanisation, trade from ports to hinterlands. It’s by no means certain that Justinian’s plague was the first, but the silk trade with China, to which the Byzantines were addicted, certainly played its part in the tragedy. Rats are handy little transporters for germs.



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  • So any-who, I wonder if there is any new development on The Berlin Patient. Quick intro from Wiki:

    Timothy Ray Brown: the 2008 cured Berlin patient[edit]
    The most famous Berlin patient is Timothy Ray Brown. He is originally from Seattle, Washington.[9] He was diagnosed with HIV in 1995 and began antiretroviral therapy. In 2006, Timothy was diagnosed with acute myeloid leukemia (AML). His physician, Dr. Gero Hütter, at Charité Hospital in Berlin, arranged for him to receive a hematopoietic stem cell transplant from a donor with the “delta 32” mutation on the CCR5 receptor.[10] This mutation, found at relatively high frequencies in Northern Europeans (16%), results in a mutated CCR5 protein.[11] The majority of HIV cannot enter a human cell without a functional CCR5 gene. An exception to this is a small minority of viruses that use alternate receptors, such as CXCR4 or CCR2.[12] Those individuals who are homozygous for the CCR5 mutation are resistant to HIV and rarely progress to AIDS. Timothy received two stem cell transplants from one donor homozygous for the delta32 mutation: one in 2007 and one in 2008.[10] Timothy stopped taking his antretroviral medication on the day of his first transplant. Three months after the first stem cell transplant, levels of HIV rapidly plummeted to undetectable levels while his CD4 T cell count increased. In addition, blood and tissue samples from areas of the body where HIV is known to hide were tested. The results were published in the New England Journal of Medicine.[10] Today, Timothy still remains off antiretroviral therapy and is considered cured.[13][14][15] Today leading HIV cure scientists agree that Timothy has what is called a sterilizing cure as opposed to a functional cure. In 2012, Timothy Ray Brown announced the formation of an organization whose sole purpose is to find a cure for AIDS called the Cure for AIDS Coalition. The first project of the Cure for AIDS Coalition is the Cure Report launched on October 16, 2014 during the NIH Strategies for an HIV Cure meeting held in the Washington, DC area.[16]

    Here’s the really cool sentence: Those individuals who are homozygous for the CCR5 mutation are resistant to HIV and rarely progress to AIDS.

    Here’s how the story goes-I just love this story-Although there are some serious arguments against it but I still love this story-So there are some sapiens, mainly from Northern European origin who have this full on mutation. The CCR5 cell receptor is knocked out. Wiki explains:

    CCR5-Δ32 is a deletion mutation of a gene that has a specific impact on the function of T cells.[24] The deleted portion of the CCR5 gene consists of thirty-two base pairs that correspond to the second extracellular loop of the receptor; the mutated receptor is non-functional and does not allow M-tropic HIV-1 virus entry, thus resulting in infection resistance.[25] One study found the frequency of the CCR5-Δ32 allele among the Caucasian population in the United States to be 0.10.[26] Another study found the allele frequency to be 0.01 for those of Western European descent; the CCR5-Δ32 allele frequency was much lower in a sampling from Venezuela.[25] A third found the frequency of the mutant allele in Caucasians of European descent to be 0.092. The same study examined DNA samples from several Western and Central African countries as well as Japan; no mutant alleles were found.[27] At least one copy of CCR5-Δ32 is found in about 4–16% of people of European descent. Two copies of the gene are found in 1% of the Caucasian population. To receive both copies, both parents would have to carry the gene.[14] It has been speculated that this allele was favored by natural selection during the Black Death for Northern Europeans, but further research has revealed that the gene did not protect against the Black Death.[28] The current hypothesis is of protection vs smallpox throughout Europe,[28] especially in the major trade cities and in isolated islands and archipelagos, such as Iceland and the Azores.[29]

    Previously we thought that it was those Northern Europeans who happened to have this particular CCR5delta32 mutation who put up some resistance to the Y pestis (plague) bacteria and then lived to reproduce. Now the mutation may give some immunity to those with this mutation to HIV virus. As the Wiki paragraphs states down at the bottom, it’s thought to be smallpox related, not Y pestis, but hey, it’s a cool story like I said above, right?!!!
    I



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  • Think I was to hard on the guy?

    Reminds me of the classic June > Ward Cleaver joke ; )

    Speaking of mammals, prairie dogs get infected by the bacteria, as if they don’t have enough problems. CDC reports some 14 cases so far this year in humans; did not know it came to the u.s. via ships to San Fran. Bay. You did mention that Bubonic plague is “tough”.



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  • I really love to tell high schoolers and other young people this story. I’ll have to update it with the new smallpox version, but I love their reaction to this because they make a connection in their minds from the present to some distant ancestors who lived hundreds of years ago who had to contend with killer pathogens just like we do today. The results of this microscopic war zone lives inside us right now! It is at this point that they tell me how much they really want to get some of that CCR5 mutation for themselves. 🙂 Great fun.



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