Of all 3,000 or 4,000 species of mosquitoes in the world, one in particular is holding an entire continent hostage.

Its name, Anopheles gambiae, recalls a narrow West African region, The Gambia, which in colonial times was known as "the white man's graveyard." Today, A. gambiae sows malaria in every region of the African continent. About 90 percent of the world's mortality from malaria, said vector biologist Frank Collins, is in sub-Saharan Africa.

As Rudyard Kipling wrote, no doubt in a different context, the female of the malaria mosquito species is more deadly than the male. It's the female that incubates the malarial parasite in her abdominal cavity; it's the female that bites her human host and injects the parasites, in exchange for a meal of blood. (See BioWorld Today Jan. 13, 1997, p. 1.)

The deadliest malarial parasite is Plasmodium falciparum.

"The malaria pandemic in the tropics," Collins observed, "is aggravated by the parasite's resistance to drugs, and the mosquito's resistance to insecticides." Curiously, the mosquito is not resistant to the parasite, although it represents a foreign body to the insect's immune system.

There's one exception. An oddball strain of the most ferocious and dangerous mosquito vector, A. gambiae, unaccountably kills rather than coddles the Plasmodia that colonize its gut.

It's like a mobster who betrays his gang by going over to the police and starts killing the killers.

This turncoat variant of the mosquito disposes of the parasites in its gut by encapsulating them in a melanotic-rich capsule * rather than cement overshoes.

"This is a strain that I selected," Collins told BioWorld Today, "that is almost a mutant, if you will. The genetic basis for why this refractory strain does this constitutes for us an entry into the twin questions: How would mosquitoes normally defend themselves? How does this wary parasite bypass this normal defense? We're interested in both sides of this question."

Collins is chief of vector genetics at the Centers for Disease Control and Prevention, in Atlanta. He is senior author of a paper in the current issue of Science, dated April 18, 1997, titled: "Quantitative trait loci for refractoriness of Anopheles gambiae to Plasmodium cynomolgi B."

"Our objective," he continued, "is at some point integrating them into some kind of malaria control."

He and his co-authors knew that the genetic basis of this strain's ability to encapsulate and kill parasites was fairly simple. In other words, it didn't take hundreds of genes, but one or only a very few. That number turned out to be three.

His collaborators at the European Molecular Biology Laboratory, in Heidelberg, Germany, developed a genetic map of the insect's genome. This suggested that three genes, one of them major, contributed to the mosquito's parasite-encapsulating activity. "Using other molecular approaches," Collins said, "we will try to see if we can incriminate one of those genes as the one responsible for this phenomenon."

He makes the point that "this is an area of interaction between a mosquito and a parasite that nobody knows about. We don't know what we're going to find, at least on a molecular level."

Collins added: "But we do have a kind of long-term malaria-control strategy in mind, which may or may not materialize in the form in which we are envisioning it."

He spelled out this strategy as being "the control of malaria transmission by genetically modifying all the wild mosquitoes so that they are no longer capable of transmitting parasites." He recalled that "in the past there have been strategies for genetic control that worked, such as release of sterile males to control the screw-worm fly in North America."

Collins concluded: "We're thinking in terms of a scenario in which a gene or genes of interest would be driven into a wild population by some kind of a drive mechanism. One analogous to an infective agent that moves through a naive population very quickly." *