HIV: the ultimate evolverEvolutionary biologists can help uncover clues to new ways to treat or vaccinate against HIV. These clues emerge from the evolutionary origins of the virus, how human populations have evolved under pressure from other deadly pathogens, and how the virus evolves resistance to the drugs we've designed. Controlling the disease may be a matter of controlling the evolution of this constantly adapting virus.
The human immunodeficiency virus (HIV, shown here budding from a white blood cell) is one of the fastest evolving entities known. It reproduces sloppily, accumulating lots of mutations when it copies its genetic material. It also reproduces at a lightning-fast rate a single virus can spawn billions of copies in just one day. To fight HIV, we must understand its evolution within the human body and then ultimately find a way to control its evolution.
Taking an evolutionary perspective on HIV has led scientists to look in three new directions in their search for treatments and vaccines:
2. Why are some people resistant to HIV?
The mutant CCR5 allele probably began to spread in northern Europe during the past 700 years when the population was ravaged by a plague. (It may have been bubonic plague or some other pathogen; research on this topic continues.) The mutant CCR5 probably made its bearers resistant to the disease, and so its frequency increased.
In some parts of Europe today, up to 20% of the population carry at least one copy of the protective allele. However, the populations of Asia and Africa were not exposed to the same epidemics; very few Asians and Africans now carry the allele (see map above). Thus, CCR5 is fairly common in northern Europe but its frequency diminishes as one moves south, and the mutation is rare in the rest of the world.
We now know that the mutant CCR5 allele has an unexpected side effect: it confers resistance to HIV. Scientists hope that studying this by-product of past selection will help them develop new treatments for the HIV epidemic ravaging human populations today.
3. How can we control HIV's evolution of resistance to our drugs?
When taking any single drug, it is fairly likely that some mutant virus in the patient might happen to be resistant, survive the onslaught, and spawn a resistant lineage.
But the probability that the patient hosts a mutant virus that happens to be resistant to several different drugs at the same time is much lower. Although multiple-drug-resistant HIV strains do eventually evolve, drug cocktails delay their evolution.
An evolutionary trade-off
Consider a patient who takes a particular drug and winds up with viruses resistant to the drug. If the patient stops taking the drug for a while, evolutionary theory predicts that her viral load will evolve back towards a non-resistant strain. If she then takes very strong doses of the drug, it may be able to halt the replication of those non-resistant viruses and reduce her viral load to very low levels.
This therapy has shown early, promising results it may not eliminate HIV, but it could keep patients' virus loads low for a long time, slowing progression of the disease.
Ultimately, understanding the evolutionary history of HIV and its pattern of evolutionary change may help us control this disease.
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Scanning electron micrograph of HIV-1 budding from a white blood cell courtesy of the CDC; Evolutionary origin of HIV diagram, adapted from Evolution: The Triumph of an Idea, by Carl Zimmer, © 2001, Harper Collins Publishers. Used with permission; Map of CCR5 frequency, adapted from Evolution: The Triumph of an Idea, by Carl Zimmer, © 2001, Harper Collins Publishers. Used with permission.
Understanding Evolution © 2016 by The University of California Museum of Paleontology, Berkeley, and the Regents of the University of California