Most historians estimate that bubonic plague killed roughly 1/3 of the population of Europe - around 25 million people. Bubonic plague first arrived in Europe in the Autumn of 1347. As the story goes, twelve Genoese galleys arrived in the port of Mecina, Sicily. Their occupants were dead or dying. The ships were immediately ordered out of the harbor, but rats carrying plague-infested fleas had already escaped onto shore. By September of 1348, the first ships carrying the Black Death arrived on the shore of England.
Bubonic plague is caused by bacteria. Bubonic plague causes large black-boils to form on the neck, armpits, and groin - the locations of major lymph nodes.
Bubonic plague is less fatal than its counterpart, Pneumonic plague. Pneumonic plague occurs when the plague bacterium spreads to the lungs, which allows the plague to be spread through the air, unlike with bubonic plague. Additionally, Pneumonic plague has a near-100% mortality rate.
Bubonic plague bacterium works by infecting white blood cells (T-cells, or lymphocytes). The purpose of white blood cells is to fight against foreign particles in the body. The bacterium attacks the cell by attaching to a "cellular gateway" which exists on all white blood cells. Interestingly, this is precisely the same method that HIV uses to bind to and infect cells.
In Europe, not everyone contracted the plague, and not everyone who contracted it died. Members of entire families were quarantined together in their homes, as became a custom when one member contracted the plague. This was generally a death sentence for all members of the household. However, there are some notable cases where one family member survived the quarantine having never contracted the plague.
Dr. Stephen J. OBrian, a geneticist, has conducted studies using the descendants of some of these survivors. These studies have demonstrated that in some communities there was a distinctly-high percentage of survivors who have a genetic mutation of the CCR5 gene. This is called the Delta-32 mutation.
The Delta-32 mutation effectively provides resistance to bubonic plague by altering the gene CCR5 in a way that prevents the plague bacterium from attaching to white blood cells. Just one copy of the Delta-32 mutation allows an individual to become sick and recover from the plague. Having two copies provides almost complete resistance.
Similar survivor-studies have been done on homosexual men who lived in the same risk-groups as those who contracted HIV in the 80's, but who never contracted the virus. AIDS has already killed roughly 18 million people worldwide. Dr. Bill Paxton, of the Aaron Diamond AIDS Research facility in New York city, has shown that a statistically-high number of these survivors also carry the Delta-32 mutation, making them resistant to HIV. Apparently, the significance of gene CCR5 as a potential avenue for therapy has been known since the mid 1990's.
Approximately 3 million people worldwide carry the Delta-32 mutation. This mutation has no doubt became more prevalant as a result bubonic plague. Those without the mutation generally died, and those with the mutation generally survived, favoring the survival of their offspring.
In conclusion, the Delta-32 mutation, and the gene CCR5, provide interesting directions for AIDS research.