An Indian-origin researcher has found that out of the 72 molecular switches that control the three key stages in the life cycle of the malaria parasite,
An Indian-origin researcher has found that out of the 72 molecular switches that control the three key stages in the life cycle of the malaria parasite, over a third of these switches can be disrupted in some way. The research by the University of Nottingham and the Wellcome Trust Sanger Institute researchers is a significant breakthrough in the search for cheap and effective vaccines and drugs to stop the transmission of the disease.
The research involved the very first comprehensive functional analysis of protein kinases in any malaria parasite. It is also the largest gene knock-out study in Plasmodium berghei - a malaria parasite infecting rodents.
"Blocking parasite transmission is recognised as an important element in the global fight to control malaria," said Rita Tewari of the University of Nottingham.
"Kinases are a family of proteins, which contribute to the control of nearly all cellular processes and have already become major drug targets in the fight against cancer and other diseases.
"Now we have identified some key regulators that control the transmission of the malaria parasite.
"Work to develop drugs to eradicate this terrible disease can now focus on the best targets.
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Oliver Billker of the Wellcome Trust Sanger Institute, said: "We can now set aside these 23 functionally redundant genes. This act of prioritisation alone has narrowed the set of targets for drug searches by a third.
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As the malaria parasite becomes increasingly resistant to existing drugs and vaccines the race to find ways of blocking the transmission of malaria is becoming increasingly important.
Last month the journal PLoS ONE published Tewari's research which identified a protein, PF16, which is critical in the development of the malaria parasite - specifically the male sex cells (gametes) - which are essential in the spread by mosquitoes of this lethal parasite.
The study, led by The University of Nottingham, found a way of disabling the PF16 protein.
The research was published in the journal Cell Host and Microbe.
Source-ANI