Viruses vs. us: A million-year-old battle
If terms like paleovirology, evolutionary biology and retroviruses cause a cloud of question marks to erupt from your head like some bewildered comic strip character, you’re not alone.
Dr. Harmit Malik explores how ancient viruses affect our vulnerability to today's diseases. (Photo by Susie Fitzhugh)
Take it from the Hutchinson Center’s Dr. Harmit Malik, one of our resident experts in these sometimes mind-bending topics. “There are no stupid questions,” he told about 90 of us—from young children to high schoolers to retirees—gathered for his lecture last week to kick off the annual Science for Life series.
By asking creative questions about our past, we’re beginning to understand why humans today—and some more than others—are susceptible to HIV, other harmful infections and even cancer. That’s the focus of work by Malik and others in an emerging research field called paleovirology—literally, the study of ancient viruses.
You may already be familiar with one of the core concepts of modern biology: Natural selection suggests that as organisms reproduce, they favor certain traits that promote survival and advancement through generations. Yet it’s clear that humans still pass down genetic mutations that put them at risk for harmful, if not deadly, diseases.
As it turns out, biologists have located evidence of a genetic double-edged sword: Some mutations produce both good and not-so-good consequences.
Consider malaria, the devastating mosquito-borne parasite that kills more people each year than almost all other diseases combined. We know that malaria disproportionately affects certain geographical bands—primarily in Africa, south Asia and parts of South America. As far back as the 1940s, scientists observed that a certain subset of these same populations are also carriers for sickle cell anemia, a genetic blood disease that harms the body’s ability to circulate oxygen, often prompting severe inflammation and organ damage.
Maybe you can see where this is going: The same genetic mutation that makes a person susceptible to sickle cell anemia also protects against malaria. That important protection may explain why this gene hasn’t simply been deleted from the human race through centuries of evolution, Malik said.
This genetic tradeoff isn’t some strange anomaly, either. Malik and his longtime mentor-collaborator Dr. Michael Emerman have discovered that human vulnerability to HIV may be explained by a different battle that humans have already won against a now-extinct, 4 million-year-old virus known as Pan troglodytes endogenous retrovirus, or PtERV.
Let’s back up a bit: First, understand that every primate, from chimpanzees and gorillas to humans, has a special protein called TRIM5α in their cells. Scientists discovered a few years ago that this protein kills HIV in rhesus monkeys—and they began wondering why it didn’t have the same effect in humans.
To tackle that question, Malik and Emerman attempted, in a sense, to reconstruct history. Using powerful computers and DNA technology, they managed to resurrect PtERV (don’t worry—they programmed it to reproduce one time only, limiting the risk for doomsday-flick scenarios). Then, through experiments with variations of the TRIM5α protein, they were able to conclude that the human variation of TRIM5α can defeat PtERV, while another version found in monkeys fights HIV.
In short, that means the same variation of TRIM5α that protected us from PtERV millions of years ago makes us more susceptible to HIV today. These opposing functions, Malik and Emerman believe, resulted from evolution.
So what about perhaps the biggest question of all—how discoveries like these may influence human health now and in the future? The hope is that new information about these ancient enemies will help scientists to engineer new treatments for our modern-day menaces.
Anne Broache
Science Writer
Editor’s note: To learn more about our scientific research without the homework, check out the three remaining free Science for Life lectures on our campus this month. The next one is Thursday, Feb. 11 at 7 p.m. Get more info here.
