ArticleScientific reports2016
The rodent malaria liver stage survives in the rapamycin-induced autophagosome of infected Hepa1-6 cells.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Host complement C3 promotes malaria transmission by killing symbiotic bacteria in the mosquito midgut.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Thioester-containing protein TEP15 promotes malaria parasite development in mosquitoes through negative regulation of melanization.Parasites & vectors · 2025Article
- Hepatocytes and the art of killing Plasmodium softly.Trends in parasitology · 2024Review
- Plasmodium's fight for survival: escaping elimination while acquiring nutrients.Trends in parasitology · 2022Review
- Malaria oocysts require circumsporozoite protein to evade mosquito immunity.Nature communications · 2022Article
- ATG Ubiquitination Is Required for Circumsporozoite Protein to Subvert Host Innate Immunity Against Rodent Malaria Liver Stage.Frontiers in immunology · 2022Article
- Review
- Plasmodium berghei sporozoites in nonreplicative vacuole are eliminated by a PI3P-mediated autophagy-independent pathway.Cellular microbiology · 2021Article
- Disrupting Plasmodium UIS3-host LC3 interaction with a small molecule causes parasite elimination from host cells.Communications biology · 2020Article
- Host cell cytosolic immune response during Plasmodium liver stage development.FEMS microbiology reviews · 2018Review
- The Interplay of Host Autophagy and Eukaryotic Pathogens.Frontiers in cell and developmental biology · 2018Review
- Shedding of host autophagic proteins from the parasitophorous vacuolar membrane of Plasmodium berghei.Scientific reports · 2017Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been reported that non-selective autophagy of infected hepatocytes could facilitate the development of malaria in the liver stage, but the fate of parasites following selective autophagy of infected hepatocytes is still not very clear. Here, we confirmed that sporozoite infection can induce a selective autophagy-like process targeting EEFs (exo-erythrocytic forms) in Hepa1-6. Rapamycin treatment greatly enhanced this process in EEFs and non-selective autophagy of infected Hepa1-6 cells and enhanced the development of the malaria liver stage in vivo. Although rapamycin promoted the fusion of autophagosomes containing the malaria parasite with lysosomes, some parasites inside the autophagosome survived and replicated normally. Further study showed that the maturation of affected autolysosomes was greatly inhibited. Therefore, in addition to the previously described positive role of rapamycin-induced nonselective autophagy of hepatocytes, we provide evidence that the survival of EEFs in the autophagosome of the infected hepatocytes also contributes to rapamycin-enhanced development of the malaria liver stage, possibly due to the suppression of autolysosome maturation by EEFs. These data suggest that the inhibition of autolysosome maturation might be a novel escape strategy used by the malaria liver stage.
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