Story by David A. Taylor
In 1999, when West Nile virus first appeared in North America, the sight of dead birds in populated areas spread fear of an epidemic that in Africa and Europe caused severe encephalitis. The virus spread rapidly in two years. And, ultimately, it reached epidemic proportions, causing 30,000 cases and more than 1,100 deaths.
The culprit seemed obvious: In Europe and Africa the virus is spread by birds, so everyone assumed that birds would spread the disease in the Western Hemisphere as well.
Now comes research by Jason Rasgon, assistant professor in the W. Harry Feinstone Department of Molecular Microbiology and Immunology, that overturns conventional wisdom and suggests that mosquitoes play a primary role in spreading the disease.
“Not much work has been done on the role of mosquitoes moving viruses across long distances,” says Rasgon, PhD. That blind spot left unexamined one of the better-traveled mosquito species, Culex tarsalis. “It’s one of the main vectors of West Nile in North America.”
“It’s an interesting mosquito,” notes Rasgon. Data gathered over more than 30 years show that C. tarsalis can travel several kilometers per night, several nights in a row. Over its lifetime, an individual mosquito’s range can match that of resident (non-migratory) bird species.
C. tarsalis has other characteristics that fit the crime. It feeds on birds and is found in rural and peri-domestic settings, so it can act as a good bridge vector when it bites humans, says Rasgon. Furthermore, it’s an extremely efficient general vector for arboviruses, including encephalitis.
To probe a possible link between the spread of West Nile virus and C. tarsalis, Rasgon and his collaborators collected mosquitoes from 20 populations across the U.S. They examined the mosquitoes’ genetic structure and found three defined clusters of populations in the U.S.—from the Midwest to West and Southwest—with limited gene flow among them. Those clusters fit the pattern of the virus spread.
Looking back, the period between 2001 and 2002, when the virus crossed the Mississippi, helped point to C. tarsalis. The east-west movement didn’t fit the north-south pattern of bird migration. “We’re not saying birds aren’t involved,” says Rasgon, “but mosquitoes have a role.”
Rasgon and colleagues published their study in the March 2 issue of Molecular Ecology.
“I was expecting varied reactions,” says Rasgon, but he was pleasantly surprised. Most responses have been positive, with scientists agreeing with the conclusion that a connection between mosquito populations and the disease should be further examined.
Rasgon still hopes to identify specific C. tarsalis genes responsible for virus transmission “to understand what makes it such an efficient vector.” The Molecular Ecology study was retrospective, tracking the disease after the fact. “We’d like to be able to do this prospectively, and anticipate a disease’s spread. If an introduced virus follows corridors of mosquito gene flow, we might be able to predict how it will spread by examining mosquito population genetics. That’s something we’re actively working on.”
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