Although public health efforts have eradicated some diseases and helped limit the impact of many others, malaria continues to present a massive public health issue. A large fraction of the world's population lives in areas where the parasite poses a risk, and it kills a million people annually, most of them in the developing world.
The malarial parasite, Plasmodium, has proven tough to tackle for a variety of reasons. Once in a human, it manages to change the proteins that cover its surface often enough that our immune systems have trouble mounting a successful response. Unlike a bacteria or virus, the parasite is a eukaryote, just like humans, which means that it's harder to find unique biochemical properties that would let us target it with drugs. Plasmodium has also been able to evolve resistance to the few drugs that we've been using to treat it. That evolution of resistance extends to its vectors, a few species of mosquitos, which have also evolved resistance to many of the pesticides we have used to keep them in check.
All of that might seem to be enough to make tackling malaria seem like an intractable problem. But some researchers are reporting some success with a new approach to limiting its spread: engineering a mosquito parasite to attack it before it can reach humans.
The species of mosquitos that transmit malaria are themselves vulnerable to parasites, including some forms of fungus. This has led to interest in using these fungi as a form of biological insecticide. But the fungus doesn't always kill quickly enough, and if it did, it might end up facing the same sorts of problems that chemical insecticides do: the mosquitos would simply evolve resistance to the fungus as well.
The solution the researchers arrived at is to use a form of fungus that doesn't kill the mosquitos until late in their lives, after they've had a chance to reproduce. This keeps them from evolving resistance, but wouldn't keep them from spreading Plasmodium. To do that, they turned to a bit of genetic engineering, creating fungi that produce various proteins that attack the parasite.
The authors tried a variety of approaches. These parasites exit the mosquito through its salivary gland, so the authors created a modified protein that coated the glands, blocking Plasmodium's attempts to latch on to them. They also used a fragment of an antibody that binds directly to Plasmodium's, as well as a toxin present in scorpion venom that kills it. They merged two of the approaches, fusing the venom protein to the one that coats the salivary gland.
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