A chance discovery by scientists may provide new ways to tackle the parasite responsible for malaria.
The malaria parasite, which is transmitted to humans through the bites of infected mosquitoes, survives within our red blood cells. It has increasingly developed resistance to nearly every antimalarial drug we use today, leading to a lack of treatments.
Experts at St George’s, University of London, have been investigating this process and during some routine laboratory experiments, they unexpectedly identified malaria parasites with greatly enlarged food vacuoles. These are structures which the parasites use to digest the contents of their red blood cell homes, which is mostly haemoglobin.
The cause of the enlarged vacuoles was found to be a mutated version of a protein called PfCRT, which is already known to play a critical role in the malaria parasite’s resistance to the old antimalarial drug chloroquine. This drug was once the frontline antimalarial drug used around the world. Now it is all but useless due to the spread of chloroquine-resistant malaria parasites.
These newly identified malaria parasites, carrying the mutated PfCRT, were more sensitive to chloroquine rather than being more resistant. These findings provide new insight into the function of PfCRT in antimalarial drug resistance and encourage new studies to find drugs that can reverse chloroquine resistance by targeting PfCRT. Ultimately, this may lead to the reintroduction of chloroquine as a treatment for malaria.
Dr Henry Staines, co-author of the report, said: “At the moment, chloroquine is effectively useless. However, our greater understanding of how it works and its present lack of clinical use, which has led to parasites losing their resistance, may mean that this cheap and well tolerated drug could still prove extremely useful in our fight to eradicate malaria. This work is a stepping stone to achieving this globally important goal.”
The study led by Dr Henry Staines and Professor Sanjeev Krishna and has been published in the journal Scientific Reports.
Mutations in the Plasmodium falciparum chloroquine resistance transporter, PfCRT, enlarge the parasite’s food vacuole and alter drug sensitivities