Health & Medicine - Posted by Dennis O'Shea-JHU on Tuesday, April 3, 2012 8:56 - 1 Comment
Dengue turns mosquitoes into eating machines
JOHNS HOPKINS (US) — Dengue virus infection triggers genes that make mosquitoes hungrier, better at smelling hosts to feed on, and perhaps more likely to spread disease to human populations.
Researchers say infection of the mosquito with a dengue fever-causing virus turns on genes that regulate the insect’s immune system, feeding behavior, and ability to sense odors.
“Our study shows that the dengue virus infects mosquito organs, the salivary glands, and antennae that are essential for finding and feeding on a human host,” says George Dimopoulos, professor at the Malaria Research Institute at Johns Hopkins University. “The virus may, therefore, facilitate the mosquito’s host-seeking ability.”
This Aedes aegypti mosquito is infected with dengue virus in its antennae and palp—both chemosensory organs—and its feeding organs, or proboscis. (Credit: George Dimopoulos, Johns Hopkins University.)
Straight from the Source
Although scientists do not yet fully understand how feeding efficiency affects virus transmission, Dimopoulos says, the genetic changes theoretically could increase transmission efficiency.
“In other words,” he says, “a hungrier mosquito with a better ability to sense food is more likely to spread dengue virus.”
Dengue virus is primarily spread to people by the mosquito Aedes aegypti. Over 2.5 billion people live in areas, primarily tropical and sub-tropical, where dengue fever is endemic.
The World Health Organization estimates that there are between 50 million and 100 million dengue infections each year. A relatively small number of those infected develop dengue hemorrhagic fever, a severe, potentially fatal form of the disease, the National Institutes of Health says.
The Johns Hopkins researchers, whose findings were published March 29 in PLoS Pathogens, performed a genome-wide microarray gene expression analysis of dengue-infected mosquitoes.
The test showed that infection regulated 147 genes with predicted functions in various processes including virus transmission, immunity, blood-feeding, and host-seeking. Further analysis of infected mosquitoes showed that silencing, or “switching off,” two odorant-binding protein genes resulted in an overall reduction in the mosquito’s blood-acquisition capacity from a single host by increasing the time it took the for mosquito to probe for a meal.
“We have, for the first time shown, that a human pathogen can modulate feeding-related genes and behavior of its vector mosquito, and the impact of this on transmission of disease could be significant,” Dimopoulos says.
Funding for the research was provided by National Institute for Allergy and Infectious Disease at the National Institutes of Health.
More news from Johns Hopkins University: http://releases.jhu.edu/