ReviewFEMS microbiology reviews2018
Host cell cytosolic immune response during Plasmodium liver stage development.
Review in FEMS microbiology reviews, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Evolution of Resistance to Avian Malaria Infection in an Endemic Hawaiian Honeycreeper.Ecology and evolution · 2026Article
- Article
- Hepatocyte Autophagy in Malaria: Current Concepts, Emerging Mechanisms, and Future Therapeutic Directions.Pathogens (Basel, Switzerland) · 2026Review
- Elimination of intra-hepatocytic malaria parasites is driven by non-canonical autophagy but not nitric oxide production.iScience · 2025Article
- Plasmodium berghei liver stage parasites exploit host GABARAP proteins for TFEB activation.Communications biology · 2024Article
- Host-pathogen interactions in the Plasmodium-infected mouse liver at spatial and single-cell resolution.Nature communications · 2024Article
- Escaping the enemy's bullets: an update on how malaria parasites evade host immune response.Parasitology research · 2023Review
- Derivatives of Amaryllidaceae Alkaloid Ambelline as Selective Inhibitors of Hepatic Stage ofPharmaceutics · 2023Article
- Same, same but different: Exploring Plasmodium cell division during liver stage development.PLoS pathogens · 2023Review
- Article
- Plasmodium's fight for survival: escaping elimination while acquiring nutrients.Trends in parasitology · 2022Review
- Killing the competition: a theoretical framework for liver-stage malaria.Open biology · 2022Article
- Mid-Liver Stage Arrest ofFrontiers in cellular and infection microbiology · 2022Article
- ATG Ubiquitination Is Required for Circumsporozoite Protein to Subvert Host Innate Immunity Against Rodent Malaria Liver Stage.Frontiers in immunology · 2022Article
- Host-targeted Interventions as an Exciting Opportunity to Combat Malaria.Chemical reviews · 2021Review
- A malaria parasite phospholipid flippase safeguards midgut traversal of ookinetes for mosquito transmission.Science advances · 2021Article
- Hijacking of the host cell Golgi by Plasmodium berghei liver stage parasites.Journal of cell science · 2021Article
- Transport mechanisms at the malaria parasite-host cell interface.PLoS pathogens · 2021Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent years have witnessed a great gain in knowledge regarding parasite-host cell interactions during Plasmodium liver stage development. It is now an accepted fact that a large percentage of sporozoites invading hepatocytes fail to form infectious merozoites. There appears to be a delicate balance between parasite survival and elimination and we now start to understand why this is so. Plasmodium liver stage parasites replicate within the parasitophorous vacuole (PV), formed during invasion by invagination of the host cell plasma membrane. The main interface between the parasite and hepatocyte is the parasitophorous vacuole membrane (PVM) that surrounds the PV. Recently, it was shown that autophagy marker proteins decorate the PVM of Plasmodium liver stage parasites and eliminate a proportion of them by an autophagy-like mechanism. Successfully developing Plasmodium berghei parasites are initially also labeled but in the course of development, they are able to control this host defense mechanism by shedding PVM material into the tubovesicular network (TVN), an extension of the PVM that releases vesicles into the host cell cytoplasm. Better understanding of the molecular events at the PVM/TVN during parasite elimination could be the basis of new antimalarial measures.
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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.