ArticlePLoS pathogens2019
Trypanosoma brucei infection protects mice against malaria.
Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Immunity beyond borders: non-lethalFrontiers in immunology · 2026Article
- The relationships of viral and protozoal co-infections to Chlamydia pecorum infection and chlamydiosis outcomes in northern koalas (Phascolarctos cinereus).PLoS pathogens · 2025Article
- Mechanistic insights into the interaction between the host gut microbiome and malaria.PLoS pathogens · 2023Review
- Article
- Coinfection withJournal of tropical medicine · 2023Article
- SARS-CoV-2 decreases malaria severity in co-infected rodent models.Frontiers in cellular and infection microbiology · 2023Article
- Parasite co-infection: an ecological, molecular and experimental perspective.Proceedings. Biological sciences · 2022Article
- Impact of Dietary Protein Restriction on the Immunogenicity and Efficacy of Whole-Sporozoite Malaria Vaccination.Frontiers in immunology · 2022Article
- Excreted Trypanosoma brucei proteins inhibit Plasmodium hepatic infection.PLoS neglected tropical diseases · 2021Article
- Hematological consequences of malaria in mice previously treated for visceral leishmaniasis.Wellcome open research · 2021Article
- Possible influence of Plasmodium/Trypanosoma co-infections on the vectorial capacity of Anopheles mosquitoes.BMC research notes · 2020Article
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Authors and funding
9 authors.
Funding
Abstract
Sleeping sickness and malaria are parasitic diseases with overlapping geographical distributions in sub-Saharan Africa. We hypothesized that the immune response elicited by an infection with Trypanosoma brucei, the etiological agent of sleeping sickness, would inhibit a subsequent infection by Plasmodium, the malaria parasite, decreasing the severity of its associated pathology. To investigate this, we established a new co-infection model in which mice were initially infected with T. brucei, followed by administration of P. berghei sporozoites. We observed that a primary infection by T. brucei significantly attenuates a subsequent infection by the malaria parasite, protecting mice from experimental cerebral malaria and prolonging host survival. We further observed that an ongoing T. brucei infection leads to an accumulation of lymphocyte-derived IFN-γ in the liver, limiting the establishment of a subsequent hepatic infection by P. berghei sporozoites. Thus, we identified a novel host-mediated interaction between two parasitic infections, which may be epidemiologically relevant in regions of Trypanosoma/Plasmodium co-endemicity.
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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.