Scientists at the School of Biosciences, University of Melbourne in conjunction with Indonesia’s Eijkman Institute and Hasanuddin University, Japan’s Jichi University, Nagasaki University and Tokyo University and the US based Johns Hopkins University have recently discovered a way of preventing malarial resistance.
According to the findings of this study published in the journal Science, these group of researchers have used the malarial parasite’s own survival mechanisms to work against itself and prevent it’s further spread.
In certain parts of the world, malaria still continues to be the leading cause of death, claiming approximately 440,000 lives annually and putting 3.2 billion others at risk.
Like HIV, finding a long term cure for this disease has been close to impossible because of the parasite’s ability to mutate and resist the action of drugs. Up until now, it has also been believed that for every new drug that is targeted against this pathogen, the latter will not just change to survive but will also spread these resistance genes from one organism to another, making it’s control all the more difficult.
One such drug was Atavaquone, which was released in the year 2000 and was marketed by Glaxo Smith Kline as Malarone for use by only pregnant women and children. It’s usage was limited in fear that its widespread administration could only escalate the chances of resistance.
However, tests with infected mouse models showed that on exposure to the drug, the parasite underwent genetic changes that enabled it to naturally overcome the toxicity. These same changes, on the other hand, prevent it’s survival in the mosquito vector and die before reaching its salivary gland.
So while it did manage to become resistant in one host, its failure to transfer to another helped it prevent the spread of the disease.
Out of the 44 times attempts were made to shift the resistant pathogen from one mouse model to another, only one successful result was observed. In this one particular case too, resistance was soon found to be retarded.
Professor Geoff McFadden from the School of Bioscience and one of the lead author of this study, calls this mechanism a ‘Genetic trap’. “With this trap concept, I think we can apply it to more than this pre-existing drug”.
Increasing the number of anti-malarial drugs in the market could also increase one’s access to more effective and affordable drugs.
“We might be able to change our strategy about the what kind of drugs we develop” says the scientist, who with his colleagues Dr. Dean Goodman and Dr. Vanessa Mollard has been studying the life cycle and evolution of the malarial parasite for more than six years.
These studies were re-confirmed using life threatening strains of the human malarial parasite and after the success of their lab work, these scientists are now eager to begin field trials in Kenya and Zambia very soon.
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