Researchers at the Johns Hopkins Bloomberg School of Public Health have for the first time identified a molecular pathway that triggers an immune response in multiple mosquito species capable of stopping the development of Plasmodium falciparum -the parasite that causes malaria in humans.
By silencing the gene, caspar, the researchers were able to block the development of the malaria-causing parasite in Anopheles gambiae, A. stephensi and A. albimanus mosquitoes-three mosquito species that spread malaria in Africa, Asia and the Americas. Their findings were published March 13 in PLoS Pathogens.
According to the study, the transcription factor Rel 2 is a key molecule involved in regulating several potent anti-Plasmodium defense genes that attack the parasite in the mosquito gut. Rel 2 is activated by the immune deficiency pathway (Imd) which, in turn, is negatively regulated by the caspar gene; when caspar is silenced the Rel 2 is activated. The researchers found that silencing of the caspar gene through the manipulation of gene expression resulted in mosquitoes that successfully blocked the development of Plasmodium falciparum in the gut tissue. Silencing the gene known as cactus, which is part of another pathway called Toll, was shown to have similar effect in controlling the development of Plasmodium berghei, which causes malaria in rodents.