ArticleBiology open2014
Stress granules and Plasmodium liver stage infection.
Article in Biology open, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Emerging roles of stress granules in liver diseases: a comprehensive review.Frontiers in cell and developmental biology · 2025Review
- Long non-coding RNA SNHG8 drives stress granule formation in tauopathies.Molecular psychiatry · 2023Article
- Characterization of the Gene Expression Patterns in the Murine Liver Following Intramuscular Administration of Baculovirus.Gene expression · 2021Article
- Hiding in Plain Sight: Formation and Function of Stress Granules During Microbial Infection of Mammalian Cells.Frontiers in molecular biosciences · 2021Review
- Bioenergetic regulation of microglia.Glia · 2018Review
- Malaria Parasite Liver Infection and Exoerythrocytic Biology.Cold Spring Harbor perspectives in medicine · 2017Review
- Inverted recruitment of autophagy proteins to the Plasmodium berghei parasitophorous vacuole membrane.PloS one · 2017Article
- Protein phosphorylation during Plasmodium berghei gametogenesis.Experimental parasitology · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Organisms have evolved numerous strategies to control infection by an array of intracellular pathogens. One cell autonomous pathogen control strategy is global inhibition of protein synthesis via stress granule (SG) formation. SGs are induced by stressful stimuli such as oxidative stress and nutrient deprivation, and are known to counteract both viral and bacterial infections. Pathogens, in turn, may actively block an infected cell's ability to form SGs. In vitro and in vivo, many liver stage malaria parasites are eliminated during development. We show here that SG formation is not amongst the strategies used for elimination of parasites from hepatocytes. Neither cell traversal, sporozoite invasion, nor rapid parasite growth leads to the formation of SGs. Furthermore, Plasmodium berghei infection does not compromise the ability of infected cells to assemble SGs in response to oxidative or nutritional stress. Plasmodium infection is therefore not detected by hepatocytes as a strong stressor necessitating global translational repression in response, highlighting the idea that Plasmodium has evolved strategies to ensure its remarkable growth in the hepatocyte while maintaining host cell homeostasis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.