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One of the darkest times in medieval Europe was the plague pandemic known as the Black Death, which killed at least 25 million people in just five years. However, the illness did not stop there. The plague has been adapted to keep hosts alive for longer, and it could continue to spread over centuries and infect people, and researchers now say they have discovered how to do that.
The disease is caused by the yersinia pestis bacteria, which are circulating among a population of at least 5,000 years. The pathogen has fueled three major plague pandemics since the first century AD, and while its deadly years appear to be behind us, the plague has not disappeared. In Asia, South America and the US, cases occur several times a year, more commonly in parts of Africa. According to the Cleveland Clinic, it can be treated with antibiotics.
Scientists are still searching for answers on how Y. Pestis evolved and dispersed, but recent analysis of ancient and modern Y. Pestis samples revealed how the plague lasts among humans for hundreds of years since the pandemic wave became Peter. A study published Thursday in the journal Science found that high infection rates and killing infected people within three days produced new strains that were transformed into just one gene, resulting in a more deadly and contagious new strain.
These weakened strains eventually became extinct. The dominant lineage of Y. pestis today is a deadly variety, the study authors reported. However, these findings on historical cases of Y. Pestis’ adaptation may provide important clues to help scientists and doctors manage the modern outbreak of plague.
The most common form of plague is the plague of foam, which causes painful swelling in the lymph nodes, spreading among people through bites from hitchhiking fleas in infected rats. The outbreak of the foam epidemic in Europe between 1347 and 1352 led to approximately 30-50% of the continent’s population becoming famous. However, the earliest known outbreak of the Justinian plague took hold in the Mediterranean basin and continued from 541 AD to 544 AD.
For new research, scientists collected ancient samples of human Y. pestis, dating back about 100 years after the emergence of the first and second plague pandemics, and the sampling remained from Denmark, Europe and Russia. After reconstructing the genomes of these plague strains, they compared them with old ancient strains that date back to the beginning of the plague pandemic.
Researchers also looked at more than 2,700 genomes of the latest plague samples in Asia, Africa, North and South America. Jennifer Klunk, one of the study’s co-authors, is a product scientist at Daciel Arbor Biosciences, a Michigan biotechnology company, and provided synthetically created molecules for the experiments, but did not have the economic benefits associated with the study.
Researchers have discovered that their newly reconstructed genomes have few copies of the gene called PLAs from the first two plague pandemics from 100 years, For decades, this has been recognized as one of the factors that have made the plague so deadly, according to Ravneet Sidhu, a doctoral student at McMaster Ancient DNA Centre at McMaster University, Ontario, Canada.
Plastic It encodes enzymes that interact with host proteins. “And one of the functions it does is break down the blood clot,” Sidhu told CNN. This ability is Y. Helps the Pestis spread to the host lymph nodes, where it replicates the rest of the body before attacking.
“Not all functions of this gene are fully known,” added Sidhu. However, previous studies by other researchers have linked PLA to the severity of the disease caused by both glandular and pneumonia plague. This is a form of airborne illness that affects the lungs, she said.
The reconstructed strain showed fewer copies of the PLA gene, but scientists were still unclear whether it would directly affect how fatal the disease is. So they tested a declined PLA strain We found that the survival rate of this type of plague was 10-20% higher in these experimental subjects than in mice infected with Y. pestis, which had normal amounts of plague. gene. Also, the tension in the reconstructed bubbles lasted for about two days, killing the host.
“This paper presents a strong argument that depletion of PLA (an enzyme produced by the PLA gene) is not a total loss, but a part of the evolution of plague pathogens, and helps explain the decline of the second pandemic plague, commonly known as black death.” Anderson, who was not involved in the new study, is investigating the pathogenicity of the plague, and these findings could shed light on transmission patterns in modern cases, she told CNN via email.
“In our lab, we have collaborators who study the routen cycle of fleas and do field research in areas where they experience annual or occasional plague outbreaks in the wild,” Anderson said.
“There are nearly 300 rodents that can infect Yersinia Pestis, but today, pile-draining rodents such as prairie dogs and ground squirrels are considered important animal hosts to experience the outbreak of disease,” she added. “After reading this paper, we will pay close attention to the PLA in the future to see if the role of that representation continues to play a role in promoting an explosive outbreak of animal population epidemics.”
The mathematical model suggested how this unfolded in the population centuries ago, leading to “fast burnout” about 100 years after the outbreak of the bubble epidemic.
In the early stages of the pandemic, infections were rapid, and deaths occurred quickly in both rats and humans. Over time, as the dense rat population thinned, selective pressure supported the emergence of Y. pestis’ non-fatal tension. gene. The host of rats infected with this new strain has a little more time to carry the disease and can infect more mice and more people.
“They propose models that can be easily pursued in labs that may help explain the prevalence of plague in the wild today,” Anderson said.
These weak strains of the disease eventually splashed out and became extinct. In a modern sample, researchers found only three examples of strains with reduced PLA Vietnamese genes: one from human subjects and two from black rats (ratta slattas).
“We did this very cool interdisciplinary study between modern and ancient data and were able to marry these things that have happened throughout the long evolutionary history (of the plague),” Sidhu said. “It may be interesting to see future researchers continue to try to bridge the gap between the modern third pandemic and the first and second ancient pandemics to see other similarities, because there are not many ancient pathogens with as much data as we do, like Yersinia Pestis.”
One of the rare features of Plague Pandemics is its persistence, and Y. Understanding how Pestis changed infection patterns and survived over time can shed light on the adaptation patterns of modern pandemics, such as Covid-19, she added.
“Even if you haven’t experienced the amount you were in 2020 or 2021, the pathogens are in the background. They’re still evolving.”
Mindy Weisberger is a science writer and media producer who appeared in Live Science, Scientific American and How It Works Magazine. she”The rise of zombie bugs“The Amazing Science of Parasitic Mind Control” (Hopkins Press).
