Scientists may have uncovered the cause of a deadly snake disease. It’s a virus that’s never been known to infect reptiles, and there’s a surprising link between it and the Ebola virus. NPR reports.
Inclusion body disease kills a lot of snakes all over the world. They stop eating, wither, and eventually, the disease hits their brains and nervous systems.
“Some of these snakes tie themselves into knots,” says study researcher Joseph DeRisi of the University of California, San Francisco. “They roll on their back, and they exhibit behaviors like stargazing, where they wave their heads in the sky sort of uncontrollably.”
So DeRisi’s lab extracted genetic material from sick boas, and they compared all the genes found in those boas with the genome of a healthy red-tailed boa named Balthazar (pictured).
They applied a new genetic technology called Virochip, which uses DNA microarray scanning to hunt for a suspect, Scientific American explains.
In the end, they found genetic code for a virus related to arenaviruses, which cause deadly infections in people. But they were different from all previously described arenaviruses – and none had ever been found in a reptile before.
And then, as it turns out, one of its genes is actually most closely related to the same gene as the virus that causes Ebola and fatal hemorrhagic diseases like Lassa fever, which kills thousands of people every year in Africa.
“So this virus is actually a mashup, or a genetic mix of arenaviruses and Ebola virus,” explains study coauthor UCSF’s Mark Stenglein.
The virus kills snakes but appears harmless to people. Although, the new findings could help veterinary scientists with a cure or prevention for the snake-striking variety.
The results raise two possibilities. One is that at some point snakes carried both arenaviruses and Ebola viruses, allowing them to swap genes. Another possibility, DeRisi says, is that “Ebola and arenavirus as we know them today evolved from this.”
The work was described in American Society for Microbiology’s mBio this week.
Image: UCSF news center
