Science Essays 
Book 4

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?