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AIDS, Bubonic Plague, and Human Evolution 
Stephen Darksyde, Science Writer

Science teachers are often asked by skeptical students, "Why aren't people evolving now?" The answer, of course, is that evolution works on time scales far outside of normal human experience. To witness dramatic changes in form and function would require a lifespan encompassing thousands of generations. And evolution would operate much faster if humans lived in small, isolated populations, where a new gene can take hold and spread rapidly.

Evolution has been described as "goo to you" or "monkeys to men." But viewed as genetics, evolution is simply a change in the frequency of alleles (gene variations) in a population over time, as a result of natural selection. Humans number more than six billion. It would take many generations for a single beneficial gene to become fixed into that mass of humanity, much less enough genes to turn us into a new species. But we can observe a subtle change in gene frequencies happening right now as a consequence of natural selection. It involves AIDS, a gene for the chemokine receptor, and a mutant called Delta 32. And while some of those biogenetic terms may sound intimidating, with a dab of historical context and some basic biology, the story behind them is both comprehensible and fascinating!

Around the same time that HIV was found to be fatal despite aggressive treatment of AIDS complications, physicians noticed a mysterious twist. In a minority of patients the disease progressed at a markedly slower rate. These lucky few seemed resistant, though not immune. Stranger still, when accurate tests for HIV were developed, it was found that an even smaller group infected with HIV never developed any symptoms! The race was on to find out why HIV killed most-but not all. The answer would take researchers to a surprising place and time.

Six hundred years before the first AIDS patient stumbled into an emergency room, Europe was in the grip of another epidemic, the granddaddy of them all: the Black Death. Victims developed grotesque swellings in the armpits and groin, often so severe that their skin split open and body fluids seeped out by the pint. Blood congealed in the fingertips, feet, and lips, turning them black. Death followed quickly. Within weeks, once bustling city streets were littered with decaying bodies. What medical facilities existed broke down completely. Entire sections of London and Paris were deserted as terrified residents fled to the countryside, spreading the plague to every village as they went. It was The Night of the Living Dead-only it wasn't a movie. This was real.

The suspected primary culprit of the pandemic is Yersinia pestis, a bacterium carried by fleas living on rats which permeated the large, filthy cities of the era. Y. pestis infection does result in pronounced swelling of the lymph nodes, but it doesn't explain everything. The pattern of infection, the geographic distribution of specific symptoms, and modern research on infectious disease all suggest there was more ravaging the people of Europe than a single disease.

The Black Death, also known as bubonic plague, affects the immune system. As with HIV victims, the plague patient is an easy target for opportunistic diseases: typhus, tuberculosis, smallpox, flu. What may have happened is that these diseases and others suddenly found their environment-human bodies-greatly weakened by the initial outbreak of bubonic plague initiated by Y. pestis. And like any organisms handed an opportunity to expand their domain, they radiated and evolved furiously. The result might have been a veritable stew of new superbugs able to overcome the resistance humans had developed to prior strains over thousands of generations.

Hundreds of millions died during the reign of the Black Death, and yet mysteriously, some survived infection, and others were immune. These lucky survivors were the beneficiaries of adaptations that had evolved in their genetic code.

So what does the Black Plague have to do with AIDS? Infectious pathogens gain entry to their victim's cells' by slipping through the cell membrane, a semipermeable outer wall. HIV bribes a molecular doorman called the "chemokine receptor" to get in. The blueprints for these receptors are, of course, found in our genes. In the lucky few patients who resist HIV, it was discovered that a gene involved in the construction of the chemokine receptor is defective. Constructing fewer receptors means fewer welcome mats for HIV.

This gene comes in a pair, one from each parent. If an individual has a single copy of the defective gene, there are fewer chemokine receptors on the cells, and HIV cannot infect them so easily. If both copies are defective, there are no receptors at all, and HIV is shut down cold by the body's defenses.

This life-saving genetic mutation, Delta 32, is found in higher frequencies in people with English, Scandinavian, and Germanic ancestry: the same population that took the brunt of the great plague. And as it turns out, the defective gene that we suspect conferred resistance to the Black Death all those centuries ago is the same one that gives resistance to HIV today!

In popular culture today, most people think of evolution as a fish growing legs, or monkeys turning into humans. In reality, only small changes occur from one generation to the next. But over time, those small changes add up. Eventually, the differences are large enough that an entirely new species splits off from an older parent population. Over really long periods, that process can transform a fish into an amphibian, or a tree-dwelling primate into a modern human.

Because of medical care, long generational spans, and a population in the billions, modern humans are evolving slowly, if at all. But given a big enough differential in mortality for selection to act on, we can pick up the pace as an evolving species. And more than five hundred years ago, in the midst of an epidemic that knocked off 25 percent of everyone alive, that's precisely what may have happened!

What Do You Think?

thanks i need this for my science class it helped alot. now hopefully i will get a good grade. if i do i will tell you
olivia barnett - Monday, May 11 at 13:48:34 PDT
gees I had to use this and other papers to explain to a stupid girl in my class that it was true and that people survived the plegue, she thought they all died and no person could get it now a days.
Chimi - Monday, May 18 at 07:31:18 PDT
there were more type of plagues then just bubonic... like septicemic and pneuminic. and each played a role in the deaths of those in europe
pk - Thursday, September 24 at 16:50:46 PDT
What are your references? I saw a special on this a few years back and I'm trying to write a paper for my Immunology class about it but I'm having such a difficult time finding information about this subject. It was just by luck that I stumbled upon your paper!
Harold - Tuesday, October 06 at 15:16:22 PDT
How do we explain the genetic mutation, Delta 32, only in English, German and Scandinavian populations when we all know that the bubonic plague affected every part of the globe? Is it not strange that Black people, most of whom have lived in Africa where the HIV is purported to have originated from, have not developed resistance against the virus while the opposite is true with people of Caucasian who were least exposed to the virus? If the black plague is caused by the bacterium Yersinia pestis, how does immunity against the disease become immunity to a virus (HIV) caused disease? What proof is there that the chemokine receptors in Black people have not been genetically manipulated to make their population more vulnerable to the genetically engineered HIV?
Tawanda - Thursday, October 08 at 00:50:10 PDT
I have no Chemokine receptors. My mother is mostly English and my father is from Germany. I have been giving blood samples to Yale New Haven hospital for some time now b/c my wife has AIDs, but I seem to be immune to it. Dr. Andrew Peterson believes that there may be a way to relieve our children of Chemokine at conception in the future. If anyone wants to talk about it, I have a ton of literature. Email me at cgroski@gmail.com
Chris - Wednesday, October 28 at 09:51:29 PST
Tawanda, I don't think the bubonic plague was worldwide. It definitely hit Europe, North Africa, and Asia, but I don't know if it hit worldwide, but I could be wrong. I think the reason why Delta 32 occurs in those specific populations is because of when the mutation took place. It must have taken place AFTER the humans that got to Europe left Africa. This same mutation may have occurred to Asian populations as well, but maybe it never passed on. We also know that since a large chunk of the European population does have the mutated gene, it must be a relatively old mutation (must have been passed on over many generations). The reason that black people may not have resistance is because a mutation is NOT an adaptation. It is a random event that can't be predicted of forced, for the most part. Both the black plague virus and HIV virus require breakage into the cell. The chemokine receptors that allow a bacteria or virus to do this play a crucial role in allowing this to happen. If the HIV/AIDS virus or Yersinia pestis bacteria can't break into the cell and work its magic to multiply and spread itself, then it will just get destroyed by white blood cells in the bloodstream. This is why Chris, above, is immune to HIV/AIDS. The virus can't break into his cells since there are no chemokine receptors. Lastly, are you trying to say that someone or something has genetically changed black people in Africa in order to make them more susceptible to HIV/AIDS? That is not possible. You can't force a mutation that will create chemokine receptors. Most people in the world have them, not just black people. There may be a way to genetically create a strong HIV virus that targets one group of people, but that would be cruel, and no one in their right mind who do that... I hope. Bottom line is, HIV/AIDS began when Africans ate other primate brains. Africans are more susceptible because the local population of the disease is there. Also, having one HIV allele is not bad. Having two will kill you, but having one gives you resistance to malaria, which kills a lot of Africans as well. That is how HIV is still in the population. Having one allele is actually an advantage and those people usually live on.
Sam - Tuesday, January 12 at 10:25:09 PST
there s a lot of WRONG information of the bubonic plaue here. If you have access to the internet, use it, instead of just guessing and passing along false info. First, It started in the East, was brough to Sicily and that travlled North. Second only bubonic and pmuemonic plague are the ony ones related. Pneumonic is the result of the evolution of bubonic so that it is not passed by fleas but by the sputum of one human to another. Obout one third of the Eurpoean population died, particularly those in urban areas, where they were in close contacts, and it was passed in the pneumonic form. Comparing other "plagues" to bubonic is like comparing small pox to pheumonic. lague is not a medical classification and the others are different dypes of disease.
medievalist - Sunday, July 11 at 20:21:17 PDT
there have been monkies for thousands of years if evolution is real then there would still be half evolved monkeys because they wouldn't have only started evolving in our lifetimes they would have continued evolving
nic - Friday, September 24 at 11:54:42 PDT
Nic, our monkey ancestors didn't need to become humans like us. We evolved by getting out of the trees. Out monkey cousins like it in the trees. They stayed there and adapted to their environment, as did we. Monkeys are adapting just like us, only in a different direction.
- Sunday, October 24 at 00:12:29 PDT

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