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Protection from bubonic plague. Stephens, et al. (1998), suggest that bubonic plague ( Yersinia pestis ) had exerted positive selective pressure on CCR5 Δ32. [ 43 ] This hypothesis was based on the timing and severity of the Black Death pandemic, which killed 30% of the European population of all ages between 1346 and 1352. [ 63 ]
Variants linked to protection against the 14th century bubonic plague are also associated with an increased susceptibility to autoimmune diseases. Scientists reveal how Black Death may have ...
Bubonic plague is one of three types of plague caused by the bacterium Yersinia pestis. [1] One to seven days after exposure to the bacteria, flu-like symptoms develop. [1] These symptoms include fever, headaches, and vomiting, [1] as well as swollen and painful lymph nodes occurring in the area closest to where the bacteria entered the skin. [2]
The gene affects T cell function and provides protection against HIV, smallpox and possibly plague, [51] but for the last, no explanation exists on how it would do that. However, that is now challenged since the CCR5-Δ32 gene has been found to be just as common in Bronze Age tissue samples. [52]
The human remains were found to be victims of the Great Plague of London, which lasted from 1665 to 1666. [68] In 2021, researchers found a 5,000-year-old victim of Y. pestis, the world's oldest-known, in hunter-gatherer remains in the modern Latvian and Estonian border area. [69]
The Black Death was a bubonic plague pandemic that occurred in Europe from 1346 to 1353. It was one of the most fatal pandemics in human history; as many as 50 million people [2] perished, perhaps 50% of Europe's 14th century population. [3]
The bubonic plague was the most commonly seen form during the Black Death. The bubonic form of the plague has a mortality rate of thirty to seventy-five percent and symptoms include fever of 38–41 °C (101–105 °F), headaches, painful aching joints, nausea and vomiting, and a general feeling of malaise.
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