HIV/AIDS and Darwinian evolution

Stephen Smith:

By exploring how humans evolve to win the battle with diseases and how they are sometimes vanquished by those pathogens, scientists hope to find drugs that can mimic successes and stave off the worst that viruses and bacteria can produce.

"It's a constant race between humans and their capacity to create new drugs and pathogens and their ability to evolve," said Dr. Daniel Cohen, an infectious disease researcher at Fenway Community Health in Boston, which specializes in AIDS treatment.

But before researchers can develop new drugs, they must understand the evolutionary nature of individual diseases and how viruses and bacteria, in turn, shape the evolution of humans and other animals.

Scientists have long known, for example, that in regions where malaria is common, most notably Africa, humans have developed an intrinsic defense against the parasitic illness. And that defense, which involves a change in red blood cells, has proved to be a good thing for many Africans, making them less susceptible to the disease. But the same trait has proved to be a bad thing for their descendants in the United States and other malaria-free areas, because it results in sickle cell disease, a condition that robs organs of oxygen, causing debilitating bouts of pain and sometimes death.

There are vital history lessons, too, when it comes to HIV.

As researchers unlocked the secrets of HIV, they found a gene mutation they suspect may protect against the virus that causes AIDS.

Human cells have locks on their surface -- scientists call them receptors -- and a virus must insert its key into these locks to gain entry. One of those is called CCR5, and HIV needs to unlock it to be able to infect cells. But scientists in recent years discovered that 5 to 10 percent of people in northern Europe don't have CCR5 receptors.

"And that's where the story gets interesting," said Dr. Calvin Cohen, research director for Community Research Initiative of New England, which conducts trials of AIDS drugs.

In contrast, people in Africa and Asia universally possess CCR5.

So researchers theorized that lower HIV rates in northern Europe might be due in part to some people lacking the cellular lock.

But why don't they have it? Right now, it's only an informed hunch, but scientists suspect that the mutation exhibited by northern Europeans may be an artifact of the bubonic plague. The theory goes like this: As the plague swarmed Europe starting in the 14th century, it wiped out people who possessed CCR5 but spared those who lacked it.

"What we're talking about is a Darwinian process," Harmit Malik, who specializes in the study of genetic conflict at the Fred Hutchinson Cancer Research Center in Seattle. "What was a really rare mutation was what survived. Everyone else had fallen prey to this particular pathogen."

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