A New Cellular ‘Back Door’ has been found to fight Malaria

malaria trip trna import strasbourg

Paris & Strasbourg (France) researchers have discovered an ‘Achilles Heel’ for malaria: A specific molecule the parasite needs from the host. Could this spawn a new generation of Parasitic disease drugs?

university_strasbourg_pasteur_institute_malariaMalaria is a parasitic disease that was responsible for over 400,000 deaths worldwide just in 2015, according to the WHO – especially in sub-Saharan Africa.

However, the current trend is actually a reduced number of cases worldwide (as well as related deaths), due to medical advances such as the Nobel-awarded discovery of artemisinin.

Better control of mosquito populations (Anopheles spp.) that spread the parasite are also driving this improvement (a strategy that could be helped by innovative approaches to pest control).

But research into parasitic diseases is still producing new insights into the mechanisms of infection.

This time, researchers from the University of Strasbourg and the Pasteur Institute in Paris have published in PNAS a description of how the parasite that causes malaria (Plasmodium) imports a specific molecule from its host (humans) to its own cytoplasm.

Fig. 1: The life cycle of the malarial parasite. Mosquitoes are infected by the parasites’ gametocytes during blood feeding, and then spread the sporozoites (infectious form) in other hosts.

The scientists identified a protein (tRip) localised on the surface of the cells of this protozoa (a unicellular microorganism). This tRip protein imports tRNA, a key molecule in the translation of the DNA sequence to proteins.

The discovery is fascinating on its own, as it is the first time that this kind of mechanism has been observed in the scientific community.

The authors are not yet sure of what purpose this import mechanism serves…

It may be that Plasmodium species have too few genes to code all the proteins they need, and thus would need to ‘steal’ some tRNA from its host, in order to complete the synthesis of its own proteins.

Another hypothesis is that these tRNA molecules can acts as small regulatory RNAs inside the parasite, modulating the expression of its genes in response to the infection in the host.

Fig. 2: detection of the tRip protein at the surface of a parasite’s at the sporozoite stage (left). Detection of the entry of tRNA into the sporozoite (right).

What it is known though is that if this tRip protein is inhibited, the parasite has a much slower progression – making it also interesting from a medical point of view.

For example, this protein could be a particularly good target for mRNA therapies, which ‘could take over all other biologicals in Medicine’ (being cheaper, quicker response).

This finding could even impact the therapeutic strategies for other infectious diseases as well, since the same import protein was found in other human pathogens, like Toxoplasma and Cryptosporidium (which causes respiratory and gastrointestinal illness).

So this discovery demonstrates a very curious human-host interaction, which could provide a ‘window’ to deliver novel therapies for Parasitic disease.

Featured image credit: Anopheles stephensi mosquito – CDC #5814 (Jim Gathany)
Figure 1 credit: Su et. al (2007) Genetic linkage and association analyses for trait mapping in Plasmodium falciparum. Nature Reviews Genetics (doi: 10.1038/nrg2126)
Figure 2 credit: Bour et. al (2016) Apicomplexa-specific tRip facilitates import of exogenous tRNAs into malaria parasites. PNAS (doi: 10.1073/pnas.1600476113)

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