The gene mutation found in the bacterium behind black death helped to conquer the world, say scientists

Register for CNNS Wonder Theory Science Newsletter. Explore the universe with news about fascinating discoveries, scientific progress and more.

One of the most bleak periods in medieval Europe was the plague pandemic, which is known as Black Death and was killed at least 25 million people in just five years. But the disease did not stop here. The plague that has adapted to keep their hosts alive for longer can spread and further infect people for centuries, and researchers now say that they have found out how.

The disease is caused by the bacterium Yersinia Pestis, which has been circulating among human population groups for at least 5,000 years. The pathogen has fueled three large plague pandemics since the first century AD, and although its deadliest years seem to have been behind us, Pest has not disappeared. According to the Cleveland Clinic, in Asia, South America and the United States and in parts of Africa, partly in parts of Africa in parts of Africa and can be treated with antibiotics.

Scientists are still looking for answers about how Y. Pestis has developed and distributed, but the latest analysis of the old and modern Y. Pestis samples showed how Pest managed to pass hundreds of years after pandemiew cells. After an initial period with high infection rates and a quick mortality – the killing of infected people within three days – the changes to only one gene in the bacterium produced new tribes that were less fatal and transferable, according to the research results published on Thursday in the journal Science.

These weakened tribes were finally extinct; The dominant line of today’s Y. Pestis is the more fatal variety, the authors of the study reported. However, these findings about historical cases of Y. Pestis adjustment could offer important information to help scientists and doctors to cope with modern plague outbreaks.

Trio of outbreaks

Pests is the most common form, Bubonic plague, which causes painful swelling in lymph nodes and coupled among people by bites of fleas. An outbreak of the Bubonic Pest from 1347 to 1352 in Europe, as is well known, killed about 30% to 50% of the continent population. But the earliest known Bubonic Pest outbreak – the plague of Justinian – took the Mediterranean basin and lasted from 541 AD to 544 N.

For the new study, scientists collected old rehearsals of Y. Pestis from human remains on about 100 years after the first and second plague of Pandemics, sampling from Denmark, Europe and Russia. After reconstructing the genomes of these plague trunks, they compared them with older, old trunks that went back to the beginning of the plague pandemics.

The researchers also examined more than 2,700 genome of modern plague samples from Asia, Africa and North and South America. One of the studies Co authors, Jennifer Klunk, is a product scientist at Daciel Arbor Biosciences, a biotechnology company in Michigan, which provided synthetic molecules for the experiments, but there was no financial profit in connection with research.

The researchers found outPresent For decades, this has been recognized as one of the factors that made plague as fatal as the co-lead author of the study, Ravneet Sidhu, a doctoral student of the McMaster Ancient DNA Center at MCMaster University in Ontario, Canada.

PLA encodes an enzyme that interacts with host lords, “and one of the functions it performs is the breakdown of blood clots,” Sidhu told CNN. This ability helps Y. Pestis to spread into the tavern’s lymph nodes, where it replicates before attacking the rest of the body.

“Not every function of this gene is fully known,” added Sidhu. However, earlier studies by other researchers have associated the PLA with the severity of the disease, which were caused by both Bubonic and the luminaire plague – a form of the disease that affects the lungs, she said.

While the reconstructed tribes showed fewer copies of the PLA gene, the scientists were still sure whether this would affect the fatal illness directly. Therefore, they tested the plague tribes with reduced PLA-Bubonic in mice and found that the survival rates for this type of plague were 10 to 20 percent higher in these test subjects than in mice that were infected with Y. Pestis and had a normal amount of the PLA gene. It also took the reconstructed Bubonic strain about two days longer to kill his hosts.

“The paper shows a strong argument that the exhaustion, but not the total loss of PLA (the enzyme produced by the PLA gene) is part of the development of the plague pathogen, and can help explain the decline of the plague in the second pandemic, which is generally known as a black death,” said Dr. Deborah, a professor of veterinary pathobiology, the veterinary pathobiology, that of the veteriny pathobiology at the university minor of the veterinary, at the college of the veterinary pathobiology. Anderson, who was not involved in the new research, examines the virulence of the plague, and these results could illuminate transmission patterns in modern cases, she said CNN in an e -mail.

“Our laboratory examines the flea cycle and we have employees who experience annual or occasional pest outbursts in the wild in areas where annual or occasional pestrangers experience field research,” said Anderson.

“There are almost 300 rodent species that Yersinia Pestis can transmit, and today rodents such as prairie dogs or ground squirrels are considered important animal hosts that experience illness,” she added. “After reading this paper, we will pay more attention to the PLA in the future to determine whether there is still a role in its expression in order to drive the plague in the animal populations.”

“Epidemic burnout”

Mathematical models suggested how this turned out to be in human population groups centuries ago, which led to an “epidemic burnout” about 100 years after a outbreak of the Bubonic Pest.

In the early stages of a pandemic, the infections were quick and death came quickly for rats and people. Over time, as dense rat populations, the selective pressure favored the emergence of a less fatal tribe of Y. Pestis with fewer copies of the PLA gene. With this new tribe, infected rat hosts had a little more time to carry the disease, and may enable them to infect more rats – and more people.

“They suggest a model that can be easily followed in the laboratory that can explain the spread of plague in the wild today,” said Anderson.

These weaker disease strains finally stuttered out and died out. In modern samples, the researchers found only three examples of tribes with reduced PLA genes from Vietnam: one from a human subject and two of black rats (Rattus Rattus).

“We were able to carry out this really cool interdisciplinary study between modern and old data and marry these things that have taken place throughout the long history of evolution (plague),” said Sidhu. “It could be interesting to see how future researchers continue to try to bridge this gap between modern third pandemic and the first and second old pandemics to see other similarities. Because there are not many old pathogens that we have about as much data as we do for Yersinia Pestis.”

One of the unusual characteristics of the plague pandemics is their persistence, and understanding how Y. Pestis has changed its infection patterns and survived over time could add light on the adaptive patterns of modern pandemics such as Covid-19.

“Even if we do not experience it on the amount we were in 2020 or 2021, the pathogen is in the background – still evolved and stopped.”

Mindy Weisberger is a scientific author and media producer whose work has been published in Live Science, Scientific American and How IT Works Magazine. She is the author of “Rising the zombie beetle: The surprising science of parasitic spirit control ”(Hopkins Press).

More CNN messages and newsletter create an account at CNN.com