Researchers at the Johns Hopkins Bloomberg School of Public Health have revealed that they have been able to block the development of the malaria by silencing a gene called caspar.
Research has been done in Anopheles gambiae, A. stephensi and A. albimanus mosquitoes, three mosquito species that spread malaria in Africa, Asia and the America.
The researchers revealed that caspar silencing activates the transcription factor Rel 2, a key molecule involved in regulating several potent anti-Plasmodium defence genes that attack the parasite in the mosquito gut.
They said that caspar silencing through the manipulation of gene expression resulted in mosquitoes that successfully blocked the development of Plasmodium falciparum in the gut tissue.
The team said that silencing a gene called cactus, which is part of another pathway called Toll, was also found to have similar effect in controlling the development of Plasmodium berghei, which causes malaria in rodents.
"When a mosquito is feeding on malaria-infected blood, the parasite will be recognized by the mosquito's immune system through receptors that then start the immune response. In the wild, this response is believed to occur too late to mount an efficient immune defense that would kill all parasites.
At least a few Plasmodia will successfully develop inside the mosquito and enable transmission of malaria," said Dr. George Dimopoulos, senior author of the study and associate professor at the Johns Hopkins Malaria Research Institute.
"In the lab we activated this immune response in advance of infection, giving the mosquito a head start in defeating the invading parasite," he added.
The researchers also found that Rel 2 activation did not affect the survival and egg laying fitness of the modified mosquitoes.
"This came as a pleasant surprise since it essentially means that we one day could spread this trait in natural mosquito populations using genetic modification. Furthermore, by activating Rel 2, the genetically modified mosquitoes will attack the malaria parasite with several independent immune factors, and this will make it very difficult for Plasmodium to develop resistance," said Dimopoulos.
An article on this study has been published in PLoS Pathogens.