How a Killer Virus Emerged: Changed Environment + Mutation = Evolution

It’s a medical mystery: Exactly how do emerging viruses such as SARS, HIV and hantavirus suddenly burst forth, seemingly from nowhere, to start infecting people and causing lethal diseases, sometimes in epidemic proportions?


In research that shines light on this worrisome phenomenon, a team of scientific sleuths based at the University of Texas Medical Branch at Galveston (UTMB) has examined and tested viruses from two late-20th-century outbreaks of Venezuelan equine encephalitis (VEE)—a deadly illness that can cause brain inflammation in horses and people—and compared them with a very similar virus that doesn’t tend to infect horses or people. The outbreaks occurred in 1993 and 1996 in deforested regions of the Mexican states of Chiapas and Oaxaca. In at least this case, the solution to the mystery is, as Sherlock Holmes might put it, “Evolutionary, my dear Watson.”

The scientists cite evidence suggesting that by replacing forests with ranchland along a 500-mile-long, 20- to 50-mile-wide swath of Mexico’s and Guatemala’s Pacific coastal plains, people put extreme evolutionary pressure on the strain of the VEE virus formerly prevalent there. This VEE virus previously was believed to be spread by a particular sub-species of mosquito known as Culex (Melanoconion) taeniopus as that feeds mainly on and infects rodents and other small mammals but that is not thought to be effective at transmitting the virus to horses or people to cause epidemics.

In a paper to be published in the Aug. 3 issue of the Proceedings of the National Academy of Sciences (PNAS), the researchers suggest that as deforestation wiped out the Culex sub-species, a single genetic mutation in the virus allowed it to move into a brand new niche. The mutation increased its ability to infect and be transmitted by an entirely different species of mosquitoes, called Ochlerotatus taeniorhynchus—which prefers for its blood-meal to feed on horses and other large mammals.

The virus-altering mutation was described as a single change, or substitution, in an amino-acid building block of the envelope glycoprotein. The envelope glycoprotein is the primary part of a virus that worms its way into the cells of host species via the host cells’ receptors. In addition to facilitating the virus’s infection of a new vector species (as insects and other organisms that transmit diseases are called), the researchers found that this amino acid substitution also had the effect of abruptly making the virus much more infectious and easily transmitted by this mosquito to horses and people.

No samples exist today of the VEE virus strain that once circulated between mosquitoes and small mammals in forests and swamps along the Chiapas and Oaxaca coastal plains. But the researchers had access to samples of a similar VEE virus widespread in the nearby coastal Guatemalan community of La Avellana between 1968 and 1980. By making a DNA copy of that Guatemalan virus genome, the scientists were able to prompt mutations in the lab that resulted in amino acid changes in the envelope glycoprotein. Just one of those changes in the Guatemalan virus, it turned out, controlled the infectivity of the virus for the mosquito species Ochlerotatus taeniorhynchus.

“What’s troubling,” said Professor Scott C. Weaver, director for emerging infectious diseases at UTMB’s Center for Biodefense and Emerging Infectious Diseases and senior author of the paper, “is that this shows a virus can find a simple genetic mutation that allows it to switch to a new species of mosquito that has the capacity to infect horses and people.”

“If the coastal plains were still forested, we wouldn’t have this new virus,” Weaver continued. “Environmental changes can create opportunities for viruses and other microbes to change their vectors and their host ranges. In this case, the environmental change resulted in a change in vectors to mosquitoes that are highly attracted to horses and human beings.”

VEE, like SARS, HIV and hantaviruses, is an RNA virus, meaning that its genetic material is encoded in a single-strand RNA molecule rather than the double-stranded structure characteristic of the DNA double helix. “RNA viruses have the capacity to mutate so frequently that they are able to respond very readily to new environmental opportunities we provide them or selective pressures we put on them,” Weaver said. The result is a kind of microbiological arms race in which the microbes keep pace with, or some times surge ahead of, attempts to control them.

“Many microbiologists would agree that nature is a more dangerous producer of new microbial threats than any bioterrorist ever will be,” Weaver concludes.

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