WEDNESDAY, May 7, 2003 (HealthDayNews) -- French researchers believe they've found a single mutation in the genetic code of certain mosquitoes that is responsible for their resistance to some insecticides.
The scientists claim the finding may help in developing new insecticides to combat the bugs that carry diseases such as malaria and West Nile virus.
Other experts are divided on the implications of the findings.
"We've known that this type of resistance has occurred for a while now," says Dawn Wesson, an associate professor of tropical medicine at Tulane School of Public Health and Tropical Medicine in New Orleans. "The significance here is that they've identified the actual mutation that is responsible for that resistance. So that means we might be able to devise either new or altered current insecticides that can actually overcome the mutation."
Others feel the authors of the brief, which appears in the May 8 issue of Nature, have overstated the significance of their findings.
"It does not address two major categories of insecticides that are now being used against mosquitoes -- those that are related to DDT and those that are in the pyrethroid category," says Andrew Spielman, a professor of tropical public health at the Harvard School of Public Health. "They're talking about a mutation that doesn't relate to commonly used insecticides."
According to the study authors, mosquitoes that transmit malaria and West Nile virus developed insecticide resistance more than 25 years ago in Africa, the Americas and Europe.
In normal mosquitoes, an enzyme called acetylcholinesterase lets the nerve cells recharge so they can fire up again and perform their work of sending signals to cells. Insecticides interfere with the action of acetylcholinesterase, so the insect essentially ends up dying of overstimulation, Wesson says.
The mutation occurs in a gene called ace-1, which encodes acetylcholinesterase and basically lets the mosquito dodge the effects of two families of insecticides, organophosphates and carbamates.
"The pesticide binds to the enzyme and inactivates it," says study author Mylène Weill, a lecturer in molecular biology at the University of Montpellier II in France. "The mutation prevents the insecticide from binding to the enzyme."
The researchers found this specific ace-1 mutation in 10 highly resistant strains of Culex pipiens mosquitoes from Africa, the Caribbean and Europe, and in one resistant African strain of Anopheles gambiae mosquitoes. C. pipiens carry West Nile virus and A. gambiae carry malaria, the researchers say.
The question is whether this finding will translate into any new mosquito-control strategies; Spielman is doubtful. "There is nothing in this paper that relates to that major group of compounds that are mainly used now against mosquitoes," he says.
Weill, however, is more hopeful.
"We know now the target and the mutation, so we can produce a mutated form of the enzyme and select strains for new molecules that can be active in that," she says. "We need several years but we must keep on going, finding new molecules and insecticides, otherwise at one point we will not be able to fight anymore."