It has long been known that fewer than 10 percent of any swarm of mosquitoes in the wild will transmit malaria. The conventional wisdom has been that this is just chance: a female must first bite a human unlucky enough to be infected already, then it takes about 14 days for the parasites to develop in her gut and migrate to her salivary glands, from which they exit into her next victim. Mosquitoes have short lives, and a female is usually infectious for only her last few days.

This study makes it clear that genetics play a part, too, and that mosquitoes are not just passive squirt guns for malaria parasites.

Plasmodium parasites do hurt mosquitoes, Dr. Vernick and Dr. Wirth said. They damage salivary tissue, make the mosquitoes fly less vigorously and lay fewer eggs and, to gain a toehold in the insect, may depress its immune system.

"The mosquito doesn't want to be infected, so it has responded with this very powerful mechanism," Dr. Vernick said, referring to what he called the "resistance island" on the mosquito genome.

By a very different route, the fungus also weakens mosquitoes; they fly badly and bite less, and many die within 14 days. For unknown reasons, it weakens plasmodium-carrying mosquitoes more than it does others, Dr. Vernick said, so if a strain of the fungus just strong enough to kill off old, weak, malarial mosquitoes could be developed, it could "tip the balance," he said. It would suppress the malaria-susceptible mosquitoes without creating mutation pressure on all mosquitoes to evolve a fungus-resistant form, as DDT created pressure to evolve pesticide-resistant forms.

For the study, scientists from the University of Minnesota, the University of Bamako in Mali, the Fred Hutchinson Cancer Research Center in Seattle and Princeton University collected wild anopheles gambiae mosquitoes, the species most likely to spread malaria in Africa, in villages in Mali.

They let each produce a generation of offspring, then let them suck malaria-infected blood (drawn from a villager, but fed through a plastic membrane). A week later, they dissected them to see where the parasites grew. They were surprised to find that 22 percent had no parasites at all, and that many others had low numbers. Then they compared mosquito genomes and narrowed the search with a gene they named APL1. When they disabled it, they found that parasites grew well.