ArticleInfection and immunity2001
Interaction between host complement and mosquito-midgut-stage Plasmodium berghei.
Article in Infection and immunity, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 64 citations in OpenAlex.
- Phase 1 vaccine trial of Pvs25H: a transmission blocking vaccine for Plasmodium vivax malaria.Vaccine · 2005Trial
- Host macrophages/monocytes promote malaria transmission by modulating mosquito microbiota via SR-A-mediated phagocytosis.Nature communications · 2026Article
- A paternal lactate dehydrogenase critically enhances male gametogenesis and malaria transmission.Scientific reports · 2025Article
- 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
- Plasmodium falciparum Gametes and Sporozoites Hijack Plasmin and Factor H To Evade Host Complement Killing.Microbiology spectrum · 2023Article
- Vector microbiota manipulation by host antibodies: the forgotten strategy to develop transmission-blocking vaccines.Parasites & vectors · 2022Review
- C-type lectin 4 regulates broad-spectrum melanization-based refractoriness to malaria parasites.PLoS biology · 2022Article
- Blood Meals With Active and Heat-Inactivated Serum Modifies the Gene Expression and Microbiome ofFrontiers in microbiology · 2021Article
- Last-come, best served? Mosquito biting order andProceedings. Biological sciences · 2020Article
- Transcriptome of theInternational journal of molecular sciences · 2020Article
- Complement in malaria: immune evasion strategies and role in protective immunity.FEBS letters · 2020Review
- Characterization of a Sulfhydryl Oxidase FromFrontiers in cellular and infection microbiology · 2020Article
- Human C5a Protein Participates in the Mosquito Immune Response Against Dengue Virus.Journal of medical entomology · 2016Article
- Malaria Parasites: The Great Escape.Frontiers in immunology · 2016Review
- An. gambiae gSG6-P1 evaluation as a proxy for human-vector contact in the Americas: a pilot study.Parasites & vectors · 2015Article
- Dengue Virus Infection of Aedes aegypti Requires a Putative Cysteine Rich Venom Protein.PLoS pathogens · 2015Article
- The cell biology of malaria infection of mosquito: advances and opportunities.Cellular microbiology · 2015Review
- Anopheles midgut epithelium evades human complement activity by capturing factor H from the blood meal.PLoS neglected tropical diseases · 2015Article
- Effects of ingested vertebrate-derived factors on insect immune responses.Current opinion in insect science · 2014Article
- The Plasmodium bottleneck: malaria parasite losses in the mosquito vector.Memorias do Instituto Oswaldo Cruz · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
After ingestion by mosquitoes, gametocytes of malaria parasites become activated and form extracellular gametes that are no longer protected by the red blood cell membrane against immune effectors of host blood. We have studied the action of complement on Plasmodium developmental stages in the mosquito blood meal using the rodent malaria parasite Plasmodium berghei and rat complement as a model. We have shown that in the mosquito midgut, rat complement components necessary to initiate the alternative pathway (factor B, factor D, and C3) as well as C5 are present for several hours following ingestion of P. berghei-infected rat blood. In culture, 30 to 50% of mosquito midgut stages of P. berghei survived complement exposure during the first 3 h of development. Subsequently, parasites became increasingly sensitive to complement lysis. To investigate the mechanisms involved in their protection, we tested for C3 deposition on parasite surfaces and whether host CD59 (a potent inhibitor of the complement membrane attack complex present on red blood cells) was taken up by gametes while emerging from the host cell. Between 0.5 and 22 h, 90% of Pbs21-positive parasites were positive for C3. While rat red and white blood cells stained positive for CD59, Pbs21-positive parasites were negative for CD59. In addition, exposure of parasites to rat complement in the presence of anti-rat CD59 antibodies did not increase lysis. These data suggest that parasite or host molecules other than CD59 are responsible for the protection of malaria parasites against complement-mediated lysis. Ongoing research aims to identify these molecules.
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