Evolution Research - General Evolution News

When man made his way out of Africa some 60,000 years ago to populate the world, he was not alone: He was accompanied by the bacterium Helicobacter pylori, which causes gastritis in many people today. Together, man and the bacterium spread throughout the entire world. This is the conclusion reached by an international team of scientists led by Mark Achtman from the Max Planck Institute for Infection Biology in Berlin, Germany. The researchers also discovered that differences developed in the genetic makeup of the bacteria populations, just as it did in that of the various peoples of the world. This has also given scientists new insight into the paths taken by man as he journeyed across the Earth.

The migration paths taken by modern man as he colonized the world. 60,000 years ago, Homo sapiens left his original home in East Africa - taking the bacterium Helicobacter pylori with him. The abbreviation kyears stands for thousand years. Image: Max Planck Institute for Infection Biology

More than half of all human beings are infected with Helicobacter pylori, a bacterium that can cause stomach ulcers. Like humans, the bacteria are also split up into numerous regional populations. A team of scientists led by Mark Achtman at the Max Planck Institute for Infection Biology, François Balloux at the University of Cambridge and Sebastian Suerbaum at Hanover Medical University have found signs of the parallel evolution of man and H. pylori. Using mathematical simulations, the researchers demonstrated that H. pylori must have left East Africa at the same time as man - around 60,000 years ago. This astonishing conformity was uncovered by scientists when they compared the nucleotide sequencing patterns in the DNA of human and H. pylori populations.

In order to characterise the individual populations, the scientists employed the principle of isolation by distance. According to this principle, the genetic distance between two populations has a linear correlation with the length of the migration paths taken since they were separated. "It's actually quite logical," explains Dr. Mark Achtman, "because in the time that elapses after a population leaves its point of origin, the number of mutations in its genetic makeup continually increases."

However, while man was spreading throughout the world, human populations had to repeatedly pass through what scientists call genetic bottlenecks: when a population shrinks, the gene pool also becomes smaller. These losses in genetic diversity linger, even when the population starts once again to increase in number. Since the Homo sapiens populations usually had to pass through several genetic bottlenecks on their way across the globe, their genetic diversity declined the further they journeyed from their origin in East Africa.

Scientists have now uncovered similar signs of historical population migration in the genetic makeup of H. pylori. However, the genetic diversity of the bacteria is larger than that of man. This paves the way for researchers to use H. pylori data to work out the migratory movements of modern man. "The parallels between the spread of man and of H. pylori are truly astonishing," says Achtman. "This bacterium could help us attain further information on aspects of human history that are still hotly disputed today if we analyzed H. pylori in conjunction with human data." For example, after leaving East Africa, the H. pylori population spread through limited localities in southern Africa, West Africa, Northeast Africa, India and East Asia. The genes of bacteria isolated in Europe, for instance, reveal influences from Central Asia - an indication that human immigrants came to Europe from Asia.

Source: Max Planck Society PR "Out of Africa - Bacteria, as well" News B / 2007 (14) February 14th, 2007

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Based on:

An African origin for the intimate association between humans and Helicobacter pylori

Bodo Linz, François Balloux, Yoshan Moodley, Andrea Manica, Hua Liu, Philippe Roumagnac, Daniel Falush, Christiana Stamer, Franck Prugnolle, Schalk W. van der Merwe, Yoshio Yamaoka, David Y. Graham, Emilio Perez-Trallero, Torkel Wadstrom, Sebastian Suerbaum and Mark Achtman

Nature advance online publication 7 February 2007 | doi:10.1038/nature05562; Received 4 October 2006; Accepted 22 December 2006; Published online 7 February 2007

Infection of the stomach by Helicobacter pylori is ubiquitous among humans. However, although H. pylori strains from different geographic areas are associated with clear phylogeographic differentiation, the age of an association between these bacteria with humans remains highly controversial. Here we show, using sequences from a large data set of bacterial strains that, as in humans, genetic diversity in H. pylori decreases with geographic distance from east Africa, the cradle of modern humans. We also observe similar clines of genetic isolation by distance (IBD) for both H. pylori and its human host at a worldwide scale. Like humans, simulations indicate that H. pylori seems to have spread from east Africa around 58,000 yr ago. Even at more restricted geographic scales, where IBD tends to become blurred, principal component clines in H. pylori from Europe strongly resemble the classical clines for Europeans described by Cavalli-Sforza and colleagues. Taken together, our results establish that anatomically modern humans were already infected by H. pylori before their migrations from Africa and demonstrate that H. pylori has remained intimately associated with their human host populations ever since.

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Related papers:

The co-evolved Helicobacter pylori and gastric cancer: trinity of bacterial virulence, host susceptibility and lifestyle
Yusuf Akhter, Irshad Ahmed, S Manjulata Devi and Niyaz Ahmed

Infectious Agents and Cancer 2007, 2:2
doi:10.1186/1750-9378-2-2

Abstract

Helicobacter pylori is an important yet unproven etiological agent of gastric cancer. H. pylori infection is more prevalent in developing Asian countries like India and it is usually acquired at an early age. It has been two decades since Marshall and Warren (1984) first described curved bacilli in the stomach of ulcer and gastritis patients. This discovery has won them the Nobel Prize recently [2], but the debate whether H. pylori is a pathogen or a commensal organism is still hot. Associations with disease-specific factors remain illusive years after the genome sequences were made available. Cytotoxin-associated antigen A (CagA) and the so-called plasticity region cluster genes are implicated in pathogenesis of the carcinoma of stomach. Another virulence factor VacA whose role is still debatable, has recently been projected in pathology of gastric cancer. Studies of the evolution through genetic variation in H. pylori populations have provided a window into the history of human population migrations and a possible co-evolution of this pathogen with its human host. Possible symbiotic relationships were seriously debated since the discovery of this pathogen. The debate has been further intensified as some studies proposed H. pylori infection to be beneficial in some humans. In this commentary, we attempt to briefly discuss about H. pylori as a human pathogen, and some of the important issues linked to its pathophysiology in different hosts.

'We dance around in a ring and suppose, the secret sits in the middle and knows' - Robert Frost

[2] Barry J. Marshall and J. Robin Warren won the 2005 Nobel Prize in Physiology or Medicine

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Evolution of the Helicobacter pylori Vacuolating Cytotoxin in a Human Stomach

Francisco Aviles-Jimenez, Darren P. Letley, Gerardo Gonzalez-Valencia, Nina Salama, Javier Torres, and John C. Atherton

J Bacteriol. 2004 August; 186(15): 5182-5185.
doi: 10.1128/JB.186.15.5182-5185.2004.
Copyright 2004, American Society for Microbiology

Abstract

We describe two subclones of Helicobacter pylori, isolated contemporaneously from a human stomach, which differ markedly in the vacuolating cytotoxin gene, vacA, but whose near identity in sequences outside this locus implies a very recent common origin. The differences are consistent with homologous recombination with DNA from another strain and result in a changed vacA midregion and, importantly, in changed toxicity.

Excerpt

We have shown that the VacA toxin can evolve in vivo to alter its toxicity, presumably through recombination with another, unidentified, H. pylori strain. Because only two strains were identified, we cannot be certain which is the daughter, but both acquisition and loss of toxin activity within the stomach have important potential implications for pathogenesis and future clinical management strategies. For example, if H. pylori pathogenicity changes, disease expression may change, conceivably contributing to phenomena such as the waxing and waning of ulcers. One reason for developing typing systems for H. pylori based on virulence determinants such as vacA has been the hope that such strains could be identified and treated before they cause disease. If rapid evolution in vivo as demonstrated here is widespread, such a strategy would be illogical. One challenge now is to assess whether the evolution of virulence determinants such as vacA and cag is a common phenomenon, as would be predicted from the observed extent and pattern of DNA sequence diversity at other loci . That it has been demonstrated by chance in vacA in this study and in cag in a previous study would imply that such evolution is not rare.

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