Over the past 10,000 years, many deadly diseases have swept humanity, affecting some people and leaving others behind. These tragic events have left their mark on our DNA. When biologists compare modern genomes with DNA extracted from ancient bones, they can see how the frequency of genetic mutations that allow people to fight pathogens increased over millennia.
We are descendants of survivors, and our genome shows it. However, it turns out that this genetic history can be a double-edged sword.
in Works published in magazines cell genomicsThe researchers found that many of the increasing frequency of protective variants also increased the risk of autoimmune diseases, in which the immune system malfunctions. This is an interesting thought. In the course of human evolution, what saved you may return and haunt your descendants.
It was only about ten years ago that we began to recognize these changes and understand their significance. it is, Genome-wide association studies, to see if the genomes of people with a particular condition share common features. Such studies are already helping identify genetic risk factors for diseases such as macular degeneration, diabetes and rheumatoid arthritis.
The study can also look for protective gene variants. Against Presumably something like the disease that Agnolo di Tura may have suffered during the Black Death.
“What we can do is combine all this information and [have] against disease,” said study co-author Gaspard Kerner, a researcher at the Pasteur Institute in Paris.
He and other scientists are now also looking at genomes across time, so they can begin to reconstruct what happened when humans and pathogens crossed paths.
How the Plague Affects Our Genes
In a recent study, Kerner and colleagues examined the genomes of 2,879 Europeans who lived between the Neolithic period, when stone tools were first made about 10,000 years ago, and the present day. They found that many of the genetic mutations that became more common at the time were related to immunity.
Most of the changes occurred in the last 4,500 years, suggesting that we have been strongly influenced by pathogens since the Bronze Age.
Mihai Netea, professor of experimental medicine at Radboud University, says this is in line with the general idea that more concentrated living, farming and animal husbandry may have increased exposure to infectious diseases.he was involved Research suggests that the era of the disease began earlier.
The researchers found, particularly strikingly, that variants that increase the risk of infection have declined over thousands of years, while those associated with autoimmunity have increased.
Taurus Vilgaris, a geneticist who studies immune evolution at the University of Chicago, and his colleagues noticed this pattern. When investigating Black Death survival. “What protected us during the plague epidemic was a very clear trade-off today, increasing our risk of autoimmune disease,” he says.
This doesn’t necessarily mean that Bronze Age farmers who survived the plague would have developed autoimmune diseases like rheumatoid arthritis, Vilgaris noted. Environmental factors are also important, some triggering susceptibility to full-blown disease. chemicals that people may encounter at work, or certain types of infectious diseases –It may not have existed at the time.
However, it suggests that events long ago may have contributed to the rise of modern autoimmune diseases. Some estimates currently affect 1 in 10 people.
A new way to tackle autoimmune disease
Hermit Malik, an evolutionary biologist at Fred Hutchinson Cancer Center and the Howard Hughes Medical Institute, said studies like this are intriguing support for some pretty profound ideas about how survival is possible in the present danger. The genes that make
This may be partly why, after many years of natural selection, there are still extremely dangerous variants such as the deleterious BRCA1 gene associated with breast cancer, he said. Each part of our cellular machinery is a potential target for viruses, and for many years the best solutions to current problems can come with dangerous side effects.
To better understand how the mutants they flagged work in the immune system, Kerner and colleagues chose three and studied how they behaved in cells in the lab. Observed to see if it works. They got an interesting glimpse of how each variation tweaks small but important things.
For example, one modulates the body’s response to immune signals, and the other impairs the function of T cells, a type of white blood cell that helps the body fight infections. These early results suggest that studying each mutation in isolation may reveal ways to combat autoimmune disease and affect immunity, Kerner said. said.
According to Malik, each of the variants identified in the study could open new research into human immunity, both past and present.
“Each of these is a potential story of our ancestors and what compromises we made to get to where we are today,” Malik said. “I think it’s really fascinating.”
