ArticleScientific reports2020
Testing the impact of a single nucleotide polymorphism in a Plasmodium berghei ApiAP2 transcription factor on experimental cerebral malaria in mice.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 14 citations in OpenAlex.
- Low nucleotide diversity of the Plasmodium falciparum AP2-EXP2 gene among clinical samples from Ghana.Parasites & vectors · 2024Article
- Experimental vaccination by single dose sporozoite injection of blood-stage attenuated malaria parasites.EMBO molecular medicine · 2024Article
- Time of day and circadian disruption influence host response and parasite growth in a mouse model of cerebral malaria.iScience · 2024Article
- IL-15 Complex-Induced IL-10 Enhances Plasmodium-specific CD4+ T Follicular Helper Differentiation and Antibody Production.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Exploring the potential antimalarial properties, safety profile, and phytochemical composition of Mesua ferrea Linn.PloS one · 2024Article
- Article
- The origins, isolation, and biological characterization of rodent malaria parasites.Parasitology international · 2022Review
- Comparative transcriptomic analysis reveals translationally relevant processes in mouse models of malaria.eLife · 2022Article
- CCR6 expression reduces mouse survival upon malarial challenge with Plasmodium berghei NK65 strain.Memorias do Instituto Oswaldo Cruz · 2022Article
- Disease modeling and stem cell immunoengineering in regenerative medicine using CRISPR/Cas9 systems.Computational and structural biotechnology journal · 2020Review
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Authors and funding
11 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebral malaria (CM) is the deadliest form of severe Plasmodium infections. Currently, we have limited understanding of the mechanisms by which Plasmodium parasites induce CM. The mouse model of CM, experimental CM (ECM), induced by infection with the rodent parasite, Plasmodium berghei ANKA (PbANKA) has been extensively used to study the pathophysiology of CM. Recent genomic analyses revealed that the coding regions of PbANKA and the closely related Plasmodium berghei NK65 (PbNK65), that does not cause ECM, differ in only 21 single nucleotide polymorphysims (SNPs). Thus, the SNP-containing genes might contribute to the pathogenesis of ECM. Although the majority of these SNPs are located in genes of unknown function, one SNP is located in the DNA binding site of a member of the Plasmodium ApiAP2 transcription factor family, that we recently showed functions as a virulence factor alternating the host's immune response to the parasite. Here, we investigated the impact of this SNP on the development of ECM. Our results using CRISPR-Cas9 engineered parasites indicate that despite its immune modulatory function, the SNP is neither necessary nor sufficient to induce ECM and thus cannot account for parasite strain-specific differences in ECM phenotypes.
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