("Well, that's the sensational explanation. What is a bit more likely is that there may be a common virulence mechanism between Yersinia pestis and the AIDS virus, which is extremely interesting but quite different from the hypothesis that there is a mystery virus behind the Black Death.
Populations through which the Plague ran will naturally have a higher incidence of people resistant due to genetic factors because they're the ones who survived and bred. A higher incidence of resistant people means a lower incidence of AIDS, assuming that the same gene that afforded resistance to the Plague does so for AIDS.")
The mutation occurs on the gene for CCR-5, a receptor on the surface of macrophages. When a person becomes infected with HIV, the virus latches onto CCR5 and another protein — CD-4 — to be transported inside the macrophages.
CCR-5 is disabled in people with the full mutation, and so HIV is unable to gain access to the macrophages. If an individual inherits the mutant gene from both parents, they are essentially immune to HIV infection. People with one mutant and one normal gene can be infected, but tend to survive longer than infected people with two normal CCR-5 genes.
It seems as though people without the mutation, called CCR5-32, were killed by the Black Death, so that those with the mutation survived to reproduce and increase its prevalence today.
You might want to read Jesper Eugen-Olsen's research.
His team rejected the idea that the mutation became more prevalent as a result of the Black Death because the epidemic began in Sicily (in the South) and spread north to Scandinavia.
This direction of travel would have predicted that the prevalence of the mutation would have become higher in the South than in the North, which is the reverse of what actually happened.
Assuming that the mutation arose in Scandinavia, Eugen-Olsen's team concentrated on determining the time of the major spread of the mutation by examining bones found in Denmark, dating from the last Ice Age, around 8000 BC to 1950 BC. In particular, they focused on the time between 1800 and 2600 BC, a Mesolithic period of massive change and migration.
Their findings suggested that the CCR-5-32 mutation was already highly prevalent in Denmark before the Black Death.
"There is support in the fact that the distribution of the Single Grave Culture in Northern and Middle Europe matches that of the high prevalence of 32." This meant that an epidemic decimating the Stone Age population could explain the archaeological observations as well as the distribution of the 32 mutation.
They proposed that people with the genetic mutation were then more likely to survive the Black Death, passing on the mutation to current generations and conferring resistance to HIV.
On another note, a young lady was released from the hospital the other day. She had been bitten by a bat. A rabid bat. She never got the injections, and suffered through it, and lived.
The first known person in all of history to survive rabies.
A fellow I used to know got a nasty cut, and just ignored it, so I asked him.
Seems years back he had gotten ill and went to the doctor. The quack examined him and prescribed antibiotics but didn't have a clue. About 36 hours later, my friend was in intensive care, getting weaker all the time.
A visiting doctor from Seoul Korea or some such stuck his head in the door, and started screaming in Korean. When he calmed down enough, he said "tetanus".
My friend survived as well. And has lifelong immunity to tetanus.