The gene that helped fight the Black Death would now protect us from Covid-19

The gene that helped fight the Black Death would now

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    The Black Death epidemic, which caused millions of deaths in the middle of the 14th century, would have led to a genetic mutation which would have helped survivors to fight this bacterial disease. According to a British study, this genetic variation is still present in our time in some people and it would provide them with additional protection against Covid-19.

    A new British study, conducted jointly by the Universities of Bristol, Edinburgh, and Oxford, has revealed that modification of the ERAP 2 gene, which occurred in the Middle Ages to adapt to the Black Death epidemic, would still be present in the body of some human beings. Nearly 700 years later, this genetic variant would help carriers fight respiratory diseases, such as Covid-19 and pneumonia. On the other hand, this genetic composition would be linked to an increase in autoimmune diseases, such as rheumatoid arthritis and inflammatory bowel disease.

    To reach this conclusion, the researchers sought to assess whether variation in the ERAP2 gene was associated with severe infection, autoimmune disease and parental longevity. For this, they used the health data of thousands of British residents from three major databases (UK Biobank, FinnGen and GenOMICC).

    “This gene basically chops up immune system proteins”explained the lead author of the study, Dr Hamilton, a researcher from the University of Bristol in the Press release. “Although we don’t know the exact mechanism that influences disease risk, carriers of alleles that provide greater protection against respiratory disease appear to be at increased risk for autoimmune disease. This is potentially a prime example. a phenomenon called ‘balancing selection’ – where the same allele has a different effect on different diseases”.

    “It is a theoretical history of balance – linked to historical and contemporary disease profiles – that reflects our past and is rarely seen in real human examples,” adds Nicholas Timpson, professor of genetic epidemiology and co-author of the study.

    The causal link between genetics and disease susceptibility may point the way to potential treatments, the researchers conclude. “However, it also highlights potential challenges; ERAP2-targeting therapies are currently being developed to target Crohn’s disease and cancer, so it is important to consider the potential effects of these agents on infection risk.”says the study.

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