Key Takeaways
- Researchers found a genetic variant that protects against norovirus emerged with early farming in Europe about 8,000 years ago.
- The variant prevents stomach viruses from attaching to intestinal cells by rendering the FUT2 enzyme non-functional.
- While providing protection, the variant is linked to increased risks of stomach ulcers and gallstones in modern populations.
Origins of a Protective Variant
A study by researchers from Linköping University and Karolinska Institutet reveals a significant genetic discovery: a variant that shields against norovirus, commonly referred to as the winter vomiting bug, first appeared when humans transitioned to agriculture approximately 8,000 years ago. The variant originated from early farmers migrating to Europe from present-day Turkey, subsequently spreading throughout the population.
Dr. Johan Nordgren, the study’s lead author, emphasizes that understanding why specific mutations arise enhances insights into their ongoing health implications. Norovirus is highly contagious, particularly during winter months, leading to brief periods of immunity and recurrent illnesses. The research indicates that individuals who possess a specific gene variant can remain healthy when exposed to the virus.
This protective mechanism is associated with histo-blood group antigens, which are sugar molecules on mucous membranes that form a barrier against viral infections. The gene responsible for creating the FUT2 enzyme is crucial for producing these sugar molecules. Those who carry a non-functional variant of this gene lack these molecules, rendering the virus incapable of infecting intestinal cells.
Tracing Historical Spread
Led by Dr. Hugo Zeberg from Karolinska Institutet, the researchers analyzed the genomes of over 4,300 ancient humans dating back 10,000 years to trace the gene variant’s spread. Their findings indicate that with the rise of agricultural practices, increased social interactions led to more frequent viral infections, thus enhancing the selective advantage of the gene variant.
Using extensive data from biobanks, the study found that carriers of two copies of the gene variant, one inherited from each parent, rarely experience stomach-related illnesses. Furthermore, laboratory work with human “mini-guts” demonstrated that these genetically altered organoids were immune to norovirus infection.
However, this protection comes with drawbacks. Evidence suggests that carriers may face heightened risks of stomach ulcers and gallstones, a concern likely exacerbated by modern stressors and dietary habits that differ from those of early agricultural societies.
Ongoing Research and Clinical Relevance
The implications of this research extend into clinical applications. Understanding the protective nature of the gene variant can inform risk assessments for disease susceptibility. In Sweden, approximately 20 percent of the population carries two copies of this protective variant.
Dr. Nordgren’s ongoing research, backed by a grant of SEK 5,400,000 from the Swedish Research Council, will delve deeper into the relationship between blood group antigens and diseases, investigating nuances in how viruses may spread from animals to humans and the variable effectiveness of rotavirus vaccines globally.
Dr. Zeberg notes the historical significance of studying ancient DNA, likening it to a time machine that reveals the impact of ancient environmental changes on current genetic traits. This exploration into evolutionary science aims to deepen the understanding of human health and disease susceptibility across populations today.
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