Highly resistant malaria parasite infects red blood corpuscles to defend itself against the impact of anti-malarial drugs.
Of the two species of Plasmodium parasites commonly infecting humans, P. vivax grows exclusively in immature red blood cells called reticulocytes. P. falciparum can infect reticulocytes, but it grows primarily in mature red blood cells (called erythrocytes) which make up 99% of red cells in circulation.
The study shows that the different metabolic states of these human host cells provide different growth conditions for the respective parasites and warn that, as a consequence, drugs that work against one Plasmodium species might fail to be effective against the other.
After their birth in the bone marrow, red blood cells undergo a number of changes to develop into highly specialized oxygen transporters.
They expel their nucleus (with its DNA content) before they are released into the blood as reticulocytes.
As they mature they get rid of many of their other organelles as well, until they are disk-shaped cells full of hemoglobin, a red protein (which gives blood its color) designed to carry oxygen.
To address whether the two classes of host red blood cells offer different resources for parasite survival, and whether these resources could influence anti-malarial drug efficacy, researchers undertook a comprehensive biochemical analysis of the metabolites present in reticulocytes on one hand and in mature erythrocytes on the other.
They found that reticulocytes contain elevated levels of many metabolites that could potentially be scavenged by the invading and growing malaria parasite.
Researchers suggest that the availability of the reticulocyte metabolome might reduce or block the efficacy of anti-malarial drugs that target parasite metabolism.
Furthermore reticulocyte resident P. falciparum may enjoy similar protection, giving rise to the possibility that infections could re-emerge.
The study is published in PLOS Pathogens.