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Modeling Host–Vector–Pathogen Immuno-inflammatory Interactions in Malaria

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Complex Systems and Computational Biology Approaches to Acute Inflammation

Abstract

Half of the global population is at risk for malaria, which results in nearly one million deaths annually, 86 % of which are in children [1]. Plasmodium falciparum, the most important human malaria parasite, is transmitted by female Anopheles mosquitoes. Parasite development in the mosquito begins with the ingestion of blood containing sexualstage gametocytes. Mobile ookinetes penetrate the midgut epithelium 24–36 h later and transform into midgut-bound oocysts within the open circulatory system of the mosquito. Oocysts grow and develop for 10–12 days and then release thousands of sporozoites, which invade the salivary glands and are released during later blood feeding by the mosquito.

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Acknowledgments

This work was supported by NIH grant R01-AI080799.

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Correspondence to Nabil Azhar B.S. .

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Vodovotz, Y. et al. (2013). Modeling Host–Vector–Pathogen Immuno-inflammatory Interactions in Malaria. In: Vodovotz, Y., An, G. (eds) Complex Systems and Computational Biology Approaches to Acute Inflammation. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-8008-2_14

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