This disease killed 25 million people in 5 years centuries ago: Now scientists know why it’s survived all this time
The Black Death killed tens of millions in a few years. Now scientists know how the plague adapted to infect people for longer.
The Black Death spread through Europe in the 14th century across five years, killing around 25 million people. As soon as it hit, the disease was unable to be stopped, adapting itself in order to keep the hosts alive longer, giving it the perfect chance to spread farther and carry on infecting people for centuries.
For years, scientists have wondered how Yersinia pestis managed to do so with the, the bacterium having circulated among human populations for at least 5,000 years.
The plague moved quickly, infecting and spreading rapidly with mortality rates high, killing within just three days. Now scientists have revealed that changes to just one gene in the bacterium produced new strains that were less deadly and more transmissible.
Sampling remains from Denmark, Europe and Russia, scientists worked out that the bacterium, according to lead author Ravnnet Sidhu, had fewer copies of a gene called pla, the culprit behind what has made plagues so deadly in the past.
Pla, as explained by CNN, encodes an enzyme that interacts with host proteins, “and one of the functions that it carries out is in breaking down blood clots,” Sidhu added to the outlet. This ability helps Y. pestis spread into the host’s lymph nodes, where it replicates before attacking the rest of the body.
Simply put: tolerant rat hosts infected with this new strain would have a little more time to carry the disease, enabling them to infect more rats and, by consequence, more susceptible people.
Editor’s summary:
Plague has devastated human and rodent populations alike many times throughout history. Sidhu et al. tracked the genetics of virulence in the plague pathogen Yersinia pestis in ancient and modern samples. They observed that the bacterial virulence factor pla, a gene encoding a protease, periodically becomes depleted late in epidemics. The authors verified that pla depletion reduces virulence in mouse models of bubonic plague. Therefore, in response to high disease mortality, selection could act to attenuate virulence. This would allow the pathogen to persist in tolerant reservoir hosts when susceptible host populations fragment and pathogen transmission becomes uncertain. —Caroline Ash
Source: science.org
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