Scientists have documented how a single gene in the bacterium that causes bubonic plague, Yersinia pestisit was allowed to survive for hundreds of years by adjusting its virulence and the length it took to kill its victims, but these forms of plague eventually died out.
A study by researchers from McMaster University and France’s Institut Pasteur, published today in the journal Scienceaddress some fundamental epidemiologic questions: How do they enter human populations, cause rampant disease, and develop different levels of virulence to persist in populations?
The Black Death is the single deadliest pandemic in recorded human history, killing an estimated 30 to 50 percent of the population of Europe, Western Asia, and Africa as it passes through these regions. Appearing in 14Th century, it regenerated in waves over 500 years, persisting until 1840.
The Black Death was caused by the same bacteria that caused the Plague of Justinian, the first plague pandemic that broke out in the mid-500s. The Third Plague Pandemic began in China in 1855 and continues today. Its deadly effects are now more controlled by antibiotics but are still felt in regions such as Madagascar and the Democratic Republic of Congo, where cases are regularly reported.
“This is one of the first research studies to directly examine changes in an ancient pathogen, which we still see today, in an effort to understand how it evolved,” says Hendrik Poiner, director of the McMaster Ancient DNA Antiquity Chair and co-author of the study, Mikael G.
After 300 years of devastating European and Middle Eastern populations, strains of Justinian plague became extinct. Second pandemic strains emerged from infected rat populations, causing the Black Death before breaking into two major lineages. One of these two lineages is the ancestor of all present-day strains. The second re-emerged in Europe over the centuries and finally died out by the early nineteenth century.
Using hundreds of samples from ancient and modern plague victims, the team screened for a single gene. bridge, A high copy component of Y. pestis This helps it get through the immune system in the lymph nodes before spreading to the rest of the body.
An extensive genetic analysis revealed that its copy number, or total no pla Genes found in the bacterium were downregulated in subsequent outbreaks of the disease, resulting in a 20 percent reduction in its mortality and an increase in the length of its infection, meaning hosts survive longer before dying. These studies were performed in rat models of bubonic plague.
On the contrary, when pla The gene was in its original, high copy number, the disease was more controversial and killed every one of its hosts and it acted much faster.
The scientists also identified a similarity between modern and ancient stressors, which developed similar deficiencies independently. pla In the later stages of the first and second pandemics, and so far, in three samples of the third pandemic, found in Vietnam today.
In both the Justinian and Black Death niches, evolutionary change occurred approximately 100 to 100 years after the first outbreak. The scientists proposed that when the gene copy number drops and infected mice live longer, they can spread the infection further, ensuring the pathogen’s reproductive success.
“The lack of pla “Can reflect the changing size and density of rodent and human populations,” explains Powner. Humans were accidental victims. “
In cities, black rats acted as “breeding hosts” due to their high numbers and proximity to humans. Because black mice are highly sensitive Y. pestisthe pathogen needed rodent populations to survive long enough to supply new hosts Y. pestis Perpetuating and allowing the epidemic to continue.
however, plaLesser strains eventually became extinct, possibly reflecting another shift in host-pathogen relationships in their environment.
When the researchers looked for signs of decline in a large set of Third Pandemic strains preserved in a collection at the Institut Pasteur, they found three contemporary strains with three contemporaneous strains. pla deficiency
“Thanks to our international colleagues who monitor endemic plague epidemics around the world, we were able to find unique bacterial samples used for this project, which is like finding three rare needles in a haystack,” says Javier Pizarro-Serrid, director of the work, co-author of the work. Yersinia Research Unit and Contributing Center for Plague at the Institut Pasteur.
The institute has the richest collection of modern art in the world Y. pestis Isolation, adds Guillaume Moss-Feuvel, co-leader of the study and postdoctoral researcher supervised by Piezo-Sarid.
“One of the most exciting aspects of our research was the possibility of discovering a characteristic first observed in a previously extinct plague strain, which could be tested experimentally for the first time to survive in a contemporary bacterial strain.”
“Although our research sheds light on an interesting pattern in the evolutionary history of plague, it continues to circulate today in Africa, South America, and India, which were previously responsible for large-scale deaths,” says Revnet Sidhu, co-leader of the McMaster Ancient DNA Center and Ph.D. candidate.
