April 2, 2012
Dengue virus turns on mosquito genes that make them hungrier
Researchers at the Johns Hopkins Bloomberg School of Public Health have, for the first time, shown that infection with dengue virus turns on mosquito genes that make them hungrier and better feeders, and therefore possibly more likely to spread the disease to humans.
Specifically, they found that dengue virus infection of the mosquito’s salivary gland triggered a response that involved genes related to the insect’s immune system, feeding behavior and ability to sense odors. The researchers’ findings are published in the March 29 edition of PLoS Pathogens.
Dengue virus is spread to people primarily by the mosquito Aedes aegypti. More than 2.5 billion people live in areas where dengue fever is endemic, and the World Health Organization estimates that between 50 million and 100 million dengue infections occur each year.
“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. This infection induces odorant-binding protein genes, which enable the mosquito to sense odors. The virus may, therefore, facilitate the mosquito’s host-seeking ability and could—at least theoretically—increase transmission efficiency, although we don’t fully understand the relationships between feeding efficiency and virus transmission,” said George Dimopoulos, senior author of the study and a professor in the Bloomberg School’s Malaria Research Institute. “In other words, a hungrier mosquito with a better ability to sense food is more likely to spread dengue virus.”
For the study, researchers performed a genomewide microarray gene expression analysis of dengue-infected mosquitoes. 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 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 said.
The study was written by Shuzhen Sim, Jose L. Ramirez and Dimopoulos.
Funding for the research was provided by the National Institute of Allergy and Infectious Diseases.