The key finding that the parasite expropriates RNA molecules in infected cells was previously unknown. While the purpose of this host-pathogen interaction is unclear, disrupting it seems to inhibit growth of the parasite and thus this could hold a new treatment clue for developing a therapeutic agent.
Malaria is a tropical disease caused by a single-celled parasite of the genus Plasmodium. Parasites are transmitted by mosquitoes (of the genus Anopheles), in some 100 countries, presenting a risk to 3.3 billion people. The parasite infects humans via the bite of the mosquito. The parasite then travels to the liver; on maturation it reproduces in a form that infects red cells and this triggers clinical symptoms like fever. According to the World Health Organization there are some 219 million cases of malaria resulting in 660,000 deaths per year.
The parasite is difficult to kill for two main reasons. Firstly, an anti-malarial drug orientated for one parasite will not necessarily be effective against another (meaning that a different approach for malaria treatment is required.) Secondly, as with antibiotic resistant bacteria, some forms of the parasites are becoming resistant to the anti-malarial drugs.
In news about the ongoing battle against the parasite, CNRS Architecture et Réactivité de l’ARN laboratory researchers have discovered a weakness. Laboratory studies, using mice, pinpointed a protein called tRip. The protein is located on the surface of the parasite and it functions to import host cell transfer RNA into the parasite.
Importantly, when tRip is not present, the parasite is no longer capable of importing tRNA and its ability to synthesize proteins is limited and this slows down the rate of infection. The need for the host cell proteins seems to be because the parasite lacks its own proteins for growth.
Based on this discovery it should be possible to target special therapeutic molecules into the parasite, designed to disrupt this process.
The research is published in the journal PNAS and the study is headed “Apicomplexa-specific tRip facilitates import of exogenous tRNAs into malaria parasites.”
