Mechanisms of Vertebrate Host Cell Subversion by the Malaria Parasite

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Final Creative Component Paper - Woodall.pdf (235.65 KB)

Date

2022-05

Authors

Woodall, Melissa

Major Professor

Beck, Joshua

Committee Member

Beck, Joshua

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Abstract

Malaria is a life-threatening disease caused by Plasmodium parasites, which are obligate intracellular parasites, that are transmitted to humans through the bite of an infected female Anopheles mosquito. Malaria is treatable and preventable, but the prevalent global burden of this disease cannot be ignored. Current vector control strategies and therapeutic treatments have reduced the number of Malaria deaths over the last decade, but resistance to antimalarial drugs and insecticides has become a significant problem and has impacted progress toward eradication of this disease (World Health Organization, 2021). Therefore, it is important to understand and study how these obligate intracellular parasites interact with and remodel host cells to replicate and survive host immune defenses in order to improve and create effective treatments. The focus of this paper was to review current knowledge and address the following question: what mechanisms do malaria parasites use to subvert host hepatocytes and erythrocytes to establish vacuolar niches for replication, and are there different mechanisms used between hepatocytes versus erythrocytes? Overall, recent advances in technology and research techniques have revealed significant players involved in the mechanisms used by these malaria parasites for their development within their host cells, especially in relation to the blood stage of development in the human host. While the cellular interactions between the malaria intracellular parasite and the host erythrocyte have been extensively studied, knowledge about these interactions between the malaria parasite and the host hepatocyte remains very limited, and more research needs to be conducted to better elucidate these interactions.

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https://dr.lib.iastate.edu/handle/20.500.12876/105337

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