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More autoimmune diseases due to Black Death
Paolo Rossi Castelli10 Nov 20222 min read

More autoimmune diseases due to Black Death

The magazine Nature has published the results of a study on bone samples taken from the remains of people who lived before and after the 1350 pandemic. Only those who had an 'aggressive' immune system survived and passed on these features which can cause problems today.

If today part of the population is particularly at risk of developing an autoimmune disease, the responsibility also lies with the deadliest epidemic mankind has ever faced: the so-called Black Death - the plague carried by the bacterium Yersinia pestis, which killed 30 - 50% of Europe’s population in the 14th century (1346-1350) then returning several times, in successive waves, in the following centuries.

This is the conclusion of researchers from McMaster University (Canada) and the University of Chicago (USA), who have just published the results of their study of archaeogenetics in the scientific journal Nature, the same area for which the Swede Svante Pääbo won the Nobel Prize for medicine and physiology a few weeks ago.

The basic question was clear: understanding whether and how such a catastrophic event was in some way 'recorded' in the DNA of those who had experienced it, and whether it had influenced natural selection and our present-day response to disease or not. To answer it, archaeogeneticists examined 318 samples of bones and teeth from people who lived before, during, and two generations after the epidemic in London (also searching the 'plague pits' of East Smithfield, used for mass burials in 1348), and 198 samples from Denmark, in order to obtain data that was less socially and geographically restricted. The result was that there were over 400 variants of the genetic code associated with the plague among the samples taken.

Favourable mutations

In particular researchers identified certain genes (i.e. parts of the of DNA chain) involved in producing proteins that defended the body from invading pathogens and discovered that there were different versions of those genes, called alleles, that were able to protect those who possessed them, in a greater or lesser way, against the plague. Only favourable variants made it possible to overcome this terrible disease and were then passed on to the next generation by survivors.

Researchers focused on variants of a gene called ERAP2, which plays an important role in defence and concluded that those who had the most protective allele, replicated twice, were 40-50% more likely to survive.

However the 'double' variant that was favourable 700 years ago because it made the immune system more effective and aggressive, is now associated with an increased susceptibility to autoimmune diseases, in particular Crohn's disease and rheumatoid arthritis. Autoimmune diseases are caused by mistaken reactions on the part of the body's defence system, which attacks healthy cells.

Does the same principle apply to Covid 19?

"Identifying the dynamics that shaped the human immune system," explains Hendrik Poinar, coordinator of the study, "helps us understand how past pandemics, like the plague, have helped make us vulnerable to disease in modern times".
Because, underlines Poinar, a more reactive, or over-reactive, immune system makes mistakes more easily, and produces an autoimmune reaction more often.  

In the coming decades, similar studies will be carried out to see if and in what way other epidemics –more or less recent - have permanently 'shaped' our immune system. A great deal of attention will also be devoted to the effects of the SARS-CoV-2 coronavirus, which is responsible for Covid.

 

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Paolo Rossi Castelli

Journalist since 1983, Paolo has been dealing with scientific divulgation for years, especially in the fields of medicine and biology. He is the creator of Sportello Cancro, the site created by corriere.it on oncology in collaboration with the Umberto Veronesi Foundation. He collaborated with the pages of the Science of Corriere della Sera for several years. He is the founder and director of PRC-Comunicare la scienza.

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