The bacterium that led to Black Death, Yersinia pestis, can be found in many animal species and is transmitted to humans via fleas. Once transmitted, the bacterium will deliver their effector proteins into host cells through a conserved type III secretion system (T3SS), and selectively destroy immune cells like neutrophils, macrophages and dendritic cells. This process leads to rapid replication of bacteria in the host, and eventually result in host death. However, without therapy, half of the infected population would survive and develop pathogen specific antibody response, which help inhibit the replication of Yersinia pestis in the bloodstream.
The bacterium that led to Black Death, Yersinia pestis, can be found in many animal species and is transmitted to humans via fleas. Once transmitted, the bacterium will deliver their effector proteins into host cells through a conserved type III secretion system (T3SS), and selectively destroy immune cells like neutrophils, macrophages and dendritic cells. This process leads to rapid replication of bacteria in the host, and eventually result in host death. However, without therapy, half of the infected population would survive and develop pathogen specific antibody response, which help inhibit the replication of Yersinia pestis in the bloodstream.
Six hundred years after the Black Death, how is our/or the Black Death survivors’ immune system affected by this medieval tragedy? Researchers from University of Chicago recently published a Nature article which used CRISPR technology to uncovered how did Black Death shape human immune system1.
By using CRISPR gRNA library to screen for potential plague receptors involved in immune response regulation, and LentiCRISPRv2 plasmids against identified plague receptor gene, FPR1, the authors illustrated that plague did shape our immune system by selecting mutations that can confer resistance in the immune cell receptor for T3SS.
Scientists found that two regions were associated with longevity: HLA-DQA1/DRB1 (rheumatoid arthritis, negatively) and LPA (cardio-metabolism, negatively). Furthermore, studies done previously that implicated APOE, CHRNA3/5, CDKN2A/B and SH2B3 and FOXO3A were validated.
Some behaviors found to influence lifespan include smoking (negative correlation), educational attainment (positive correlation), HDL cholesterol levels (positive correlation), and body fat (negative correlation).
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