By Charlotte Hsu
To study Ebola and Marburg viruses, researchers must don airtight suits and lock themselves in a biocontainment lab, separated from the outside world by decontamination showers. The viruses cause hemorrhagic fevers in humans; victims bleed from the eyes, ears, mouth and other orifices.
Ebola and Marburg belong to a family of viruses called filoviruses. Experts once believed these lethal agents were less than 10,000 years old, but recent UB research pushed the age back—way back—to at least 10 million years.
UB biologists Jeremy Bruenn and Derek Taylor, the study’s leaders, investigate “fossil genes”: chunks of genetic material, often sizable, that animals and other organisms “steal” from viruses. The partners found remnants of filovirus genes in a lot of small mammals, including a Buffalo Zoo wallaby and a bat caught at UB. In mice and rats, the genes appeared in the same spot in the genome, meaning the material was likely acquired in ancient times, before the animals evolved as distinct species.
“A viral gene being inserted independently at the exact same position in different species is highly unlikely, so it must have happened in a common ancestor,” Taylor explains. The finding is one of many surprising results emerging from Taylor and Bruenn’s work.
Until recently, many researchers—including Taylor and Bruenn—didn’t think it was possible for filoviruses to leave their imprint on host DNA at all. That’s because filoviruses are non-retroviral RNA viruses, which lack the genetic machinery to produce reverse transcriptase, an enzyme needed for copying viral material into host genomes.
Bruenn changed his thinking in 2005, when he saw fossil genes from a non-retroviral RNA virus in two species of yeasts. “Not only were they there, but they appeared to be functional,” Bruenn recalls. “I was really intrigued: How did they get there, and why were they there?”
Now, he and Taylor are zeroing in on answers. Their research suggests that viral material gets into host DNA because of reverse transcriptase already present in the cells of the host. As for why organisms retain viral genes, Bruenn posits that doing so may confer antiviral resistance.
Moving forward, the researchers will use fossil genes to better pinpoint the age and origin of dangerous viruses. “The viral-host interaction is such an important interaction for all life on this planet, but it’s kind of a huge missing area of biology,” says Taylor. “We don’t have a lot of information about what happened in deep time.”
Since publishing on Ebola and Marburg in 2010, Bruenn and Taylor have worked with UB colleagues to identify viral remnants in a plethora of organisms, including plants and fungi. The team found that the fruit fly Drosophila has fossil genes, a notable discovery because the insects breed quickly and—like fast-replicating yeasts—could be used to study the purpose of amassing viral material.