Malaria Parasite First Inhibits Host Chemokine CXCL10 to Lessen Immune Response and Later Uses Increased Concentration of CXCL10 As Cue for Growth Acceleration and Escape to Vector Mosquito Before Host Death; Extracellular Vesicles (EVs) Play Crucial Role

In a landmark paper investigating the dynamic interplay of human host and pathogen during the course of malaria infection with Plasmodium falciparum, a team of scientists led by Neta Regev-Rudzki (photo), PhD, Senior Scientist at the Weizmann Institute of Science (Rehovot, Israel), has shown that P. falciparum first inhibits translation of the anti-parasitic host chemokine CXCL10 transcript and later, when the infection has intensified and reached the brain (cerebral malaria), uses the increasingly high CXCL10 concentration as a signal to shift growth tactics to accelerated growth and escape from the possibly dying host to continue the parasite’s life cycle in the mosquito vector. The inhibition of CXCL10 translation is orchestrated by the release, into monocytes, of RNA cargo from extracellular vesicles (EVs) secreted by Pf-infected red blood cells (RBCs). This RNA cargo inhibits CXCL10 synthesis in the monocytes by disrupting the association of host ribosomes with CXCL10 transcripts. The paper describing the team’s results was published online on August 11, 2021 in Nature Communications. The open-access article is titled “Malaria Parasites Both Repress Host CXCL10 and Use It as a Cue for Growth Acceleration.”

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