Gene Helped Overcome The Black Death, May Now Endanger Us

The Black Death, the second largest pandemic of plague, wiped out almost half of the population of Europe and North Africa. The plague ravaged Europe from his 1347 to his 1351 years, and then continued to reappear in certain areas over the centuries.

Now, an international group of scientists has analyzed DNA samples taken from the remains of plague survivors and discovered that some genes make proteins that protect the body from disease. However, these same genes are today associated with an increased risk of autoimmune diseases.

The Black Death or bubonic plague is said to have originated in the Orient.the bacterium that causes the plague called Yersinia pestis I traveled on a ship bound for the Mediterranean on a rat flea. From there it spread rapidly inland, reaching the edge of continental Europe, including Scotland, Scandinavia and the Baltics, by 1350. By rough estimates, the plague killed 25 million people across Europe.

of studywas published in Nature, examined more than 500 DNA samples from the remains of people who died before, during and after the plague, focusing on a 100-year period. They extracted samples from individuals buried in London, including East He Smithfield Plague He Pit and Denmark.

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After investigating genetic adaptations associated with the plague, scientists discovered that the Black Death is a powerful selective force that alters genetic diversity associated with the immune system.

The study, which included researchers from McMaster University, the University of Chicago, the Pasteur Institute, and other organizations, found that people with two identical versions (alleles) of the ERAP2 gene were more susceptible to the plague than those with opposites. found that they were 40% more likely to survive the disease because the “protective” version of the gene fought off pathogens much more effectively.

“In the event of such a pandemic, where 30-50% of the population would die, there is no doubt that protective allele selection in humans would occur, meaning that people susceptible to circulating pathogens would die. So even a small advantage can mean the difference between surviving or overtaking, and of course survivors in the breeding season will pass on the genes.” Hendrik Poiner saidHe is one of the authors of the paper and director of the Center for Ancient DNA at McMaster University.

But while these genes once protected people from the plague, the study suggests they are linked to making current populations more susceptible to autoimmune diseases such as Crohn’s disease, rheumatoid arthritis and lupus. showed.

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Scientists have previously attempted to find a relationship between autoimmune risk alleles and adaptation to past infections. The empirical evidence presented in the paper links the selective forces of past pandemics to current susceptibility to disease, the study notes.

Dr. Poinar said in an email explaining whether such an event could occur regarding the Covid-19 pandemic: hindu“There is certainly a selection event taking place in every pandemic, but that depends a lot on what age of the population bears the brunt of the mortality. Adults (and older people too), but these are people who could have passed on their genes but didn’t get the chance. Their genes are not excluded from the next generation because they are passed on to the next generation.”

Another factor contributing to the black plague mortality was the vulnerability of the European population. The 14th century population was not exposed. Yersinia pestis recently. As waves of the pandemic swept the continent, so did the death rate.

“We were surprised that a single pandemic was powerful enough to leave a separable imprint of natural selection on the human genome. These types of studies tell us about immune functions that have been upheld throughout evolution. Understanding such patterns is not only important from an evolutionary point of view, but can also inform us about the mechanisms and genetic determinants of susceptibility to current diseases,” said a co-author of the paper. said human geneticist Luis Barreiro, professor of genetic medicine at the university. of Chicago.