4.8 Article

Repeated out-of-Africa expansions of Helicobacter pylori driven by replacement of deleterious mutations

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NATURE COMMUNICATIONS
卷 13, 期 1, 页码 -

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NATURE PORTFOLIO
DOI: 10.1038/s41467-022-34475-3

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资金

  1. Ministry of Education, Culture, Sports, Science, and Technology (MEXT) of Japan [221S0002, 18KK0266, 19H03473, 21H00346, 22H02871]
  2. FCT [CEECIND/03023/2017, PTDC/BTM-TEC/3238/2020]
  3. National Strategic Reference Framework Operational Program Competitiveness, Entrepreneurship and Innovation (NSRF 2014-2020) [MIS5002486]
  4. InfeNeutra Project (NSRF 2007-2013) of the Ministry of Culture and Education, Greece [MIS450598]
  5. Erik Philip-Sorensen Foundation [G2016-08]
  6. Swedish Society for Medical research (SSMF)
  7. Swedish National Infrastructure for Computing (SNIC) through Uppsala Multidisciplinary Center for Advanced Computational Science (UPPMAX) [snic2018-8-24, uppstore2017270]
  8. German Research Foundation (DFG) [158 989 968-SFB 900/A1]
  9. Bavarian Ministry of Science and the Arts
  10. Shanghai Municipal Science and Technology Major Project [2019SHZDZX02]

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Helicobacter pylori has recently spread out of Africa, replacing deleterious variants that accumulated during the original out of Africa migrations more than 50,000 years ago.
Helicobacter pylori is a major human pathogen whose population structure is similar to that of its host. Here, the authors show that H. pylori has repeatedly spread out of Africa recently, replacing deleterious variants that accumulated during the original out of Africa migrations more than 50,000 years ago. Helicobacter pylori lives in the human stomach and has a population structure resembling that of its host. However, H. pylori from Europe and the Middle East trace substantially more ancestry from modern African populations than the humans that carry them. Here, we use a collection of Afro-Eurasian H. pylori genomes to show that this African ancestry is due to at least three distinct admixture events. H. pylori from East Asia, which have undergone little admixture, have accumulated many more non-synonymous mutations than African strains. European and Middle Eastern bacteria have elevated African ancestry at the sites of these mutations, implying selection to remove them during admixture. Simulations show that population fitness can be restored after bottlenecks by migration and subsequent admixture of small numbers of bacteria from non-bottlenecked populations. We conclude that recent spread of African DNA has been driven by deleterious mutations accumulated during the original out-of-Africa bottleneck.

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