Malaria still kills more than a million people a year. Even though low-tech measures such as spraying insecticides and distributing treated bed netting to residents can reduce infection rates, poor countries, where most victims live, cannot afford them.
As an alternative strategy, researchers have tried for years to genetically engineer mosquitoes so they will not transmit the disease. Malaria is caused by protozoan parasites that reproduce inside human liver and red blood cells and are passed from person to person by female Anopheles mosquitoes. Although several research teams managed to insert genes into lab-bred mosquitoes that made the bugs less hospitable to the parasites, the altered strains did not reproduce or survive as well as wild strains did.
But last March microbiologist Marcelo Jacobs-Lorena of Johns Hopkins University announced results indicating that engineered insects could outsurvive wild ones. Jacobs-Lorena inserted a gene into Anopheles that directs production of a peptide called SM1, which manifests in the mosquito's gut and prevents malaria parasites in rodents from reproducing. The Johns Hopkins team put the transgenic and natural mosquitoes in cages with malaria-infected mice, on which the mosquitoes fed. Over time the mosquitoes reproduced. After nine generations, transgenic bugs made up 70 percent of the overall population. The disease-resistant strains not only competed with the wild ones but survived better.
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The test did not prove that infection-resistance genes would spread in the wild, but it raised hope that mosquitoes doped with those genes would survive. Hardly a month later, however, biologist Bruce A. Hay of the California Institute of Technology presented evidence that engineered genes can indeed spread throughout a bug population. Working with fruit flies, Hay's team combined a segment of noncoding RNA, known as a microRNA, with a gene that was critical to the development of fruit fly embryos; the researchers then altered that gene so that it was unaffected by the RNA. Next they re-leased the fruit flies into cages with three times as many normal flies. As generations mixed, wild flies that incorporated the microRNA died because it destroyed their unprotected version of the critical developmental gene, whereas flies that bore the altered version of that gene were able to survive. After nine to 11 generations, all the offspring in the cage carried the human-made gene combination.
