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Researchers have traced the origins of a gene variant that protects humans from viral gastroenteritis — a severe intestinal infection — to early Anatolian farmers who migrated into Europe around 6,000 B.C.
The study, published in Molecular Biology and Evolution on Oct. 24 2025, analyzed the DNA of 4,343 ancient individuals spanning 10,000 years and 700,000 people today, showing how a mutation in the FUT2 gene spread across the continent during the transition to agriculture.
The FUT2 gene produces an enzyme that attaches certain sugar molecules to the surface of intestinal and respiratory cells, forming “blood group antigens” that many viruses use to infect the body. The mutation — a premature stop in the gene’s sequence — prevents production of this enzyme. Individuals inheriting two copies of the variant, known as non-secretors, are highly resistant to noroviruses and rotaviruses, the world’s most common causes of viral stomach illness.
According to the research team from Karolinska Institutet, Linköping University, and the Max Planck Institute for Evolutionary Anthropology, the mutation was virtually absent in European hunter-gatherers more than 8,000 years ago. It entered Europe with early farming communities from what is now Türkiye and rose sharply in frequency as agriculture spread. By 6000 BCE, roughly one-third of Europeans carried the variant — a level that remains similar today.
The scientists linked this rise to the sedentary, densely populated lifestyle that emerged with early farming. Close contact with livestock and limited sanitation increased exposure to gastrointestinal viruses, giving a strong evolutionary advantage to those carrying the FUT2 mutation.
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Data from large modern genetic databases — including FinnGen and the UK Biobank — confirmed that carriers of the truncation variant face a markedly lower risk of viral intestinal infections. Experiments using human intestinal organoids (miniature gut models grown from stem cells) showed that only people with two copies of the gene defect were protected, while heterozygous individuals remained vulnerable.
The findings reconcile earlier contradictions between laboratory and epidemiological studies: clinical virus samples demonstrated FUT2-dependent infection, whereas lab-cultured virus strains did not. The study also revealed that FUT2 loss of function does not protect against sapovirus, another gastrointestinal virus.
While the mutation helped ancient populations resist deadly viruses, it also carries health costs. Biobank data indicate that non-secretors have a higher risk of gallstones, duodenal ulcers, and laryngitis, as well as altered liver enzyme levels. However, no link was found between the mutation and Helicobacter pylori — the bacterium that causes many stomach ulcers — contradicting earlier, smaller studies.
Interestingly, East Asian populations developed a different FUT2 variant that provides the same viral protection but emerged several thousand years later, around 2,000 B.C. This separate evolutionary path points to similar selective pressures arising independently in different regions as humans adopted agriculture.
Lead author Hugo Zeberg of Karolinska Institutet noted that the mutation’s arrival with Anatolian farmers reflects how shifts in lifestyle — rather than climate or geography alone — can drive genetic adaptation.
The study illustrates how the spread of agriculture not only transformed human societies but also left a lasting imprint on the genome, shaping how populations respond to disease today.
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