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!
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