Proteus vulgaris, on the other hand, is an entirely boring creature. The former is better known as typhus, and for centuries it was a scourge on humanity, popping up repeatedly in crowded unsanitary situations like prisons and military camps. Start with two bacteria: Rickettsia prowazekii and Proteus vulgaris.
![proteus o x 19 proteus o x 19](https://image.slidesharecdn.com/conferenciaplticaescherichia-proteus-141103172831-conversion-gate01/95/conferencia-pltica-escherichia-proteus-52-638.jpg)
The same sort of coincidence ended up saving thousands of lives during World War II. The fact that CCR5-Δ32 also confers resistance to HIV-1 is nothing more than coincidence. If you didn’t have the mutation, you died if you did, you lived to have many children who also had the mutation. The CCR5-Δ32 mutation seems to have become common because Northern Europe was repeatedly struck by epidemics of plague (or chronically infected with smallpox, if you prefer that culprit) for centuries. Even though the two diseases act quite differently once inside the cell, they’d be similarly stymied by a change in the CCR5 receptor. In the particular case of plague bacteria, they attack the T-cells of a human’s immune system through the CCR5 receptor on the outside of those cells.
![proteus o x 19 proteus o x 19](http://2.bp.blogspot.com/-U8nlYfVj2CY/TezLwPRnsBI/AAAAAAAAABk/ojg_JXsgHGw/s1600/AAA.jpg)
The most commonly suggested culprits are smallpox and bubonic plague, both of which have been pestering people for long enough to qualify. The theory for how the mutation became so widespread involves finding another disease that uses the same point of attack as HIV-1. AIDS has been around for a lot less than that. Using a hybrid of math and genetics called coalescent theory, it’s possible to calculate that the mutation must have started to spread in the European population at least 275 years ago, with seven centuries being the likeliest figure. The peculiarity here is that the gene in question is much more common in people of Northern European descent, with somewhere between ten and fifteen percent of the population having at least one copy while it’s vanishingly rare in, say, sub-Saharan Africans or East Asians. Probably the most famous result of this is the CCR5-Δ32 mutation, one copy of which makes people resistant to HIV-1 infection two makes them almost immune.
![proteus o x 19 proteus o x 19](https://static.wixstatic.com/media/6adfd9_8e1127040f264f7385527800bdfb239a~mv2.png)
Whether due to parallel evolution or horizontal gene transfer, two bacteria use the same technique as part of their attack on a human being, with correspondingly similar results. There are sometimes odd links between two otherwise unrelated diseases.