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Heat shock proteins of malaria: Highlights and future prospects

Shonhai, A. and Blatch, G.L. (2021) Heat shock proteins of malaria: Highlights and future prospects. In: Shonhai, A., Picard, D. and Blatch, G.L., (eds.) Heat Shock Proteins of Malaria. Springer, Cham, pp. 237-246.

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The deadliest malaria parasite of humans, Plasmodium falciparum, is an obligate parasite that has had to develop mechanisms for survival under the unfavourable conditions it confronts within host cells. The chapters in the book “Heat Shock Proteins of Malaria” provide a critique of the evidence that heat shock proteins (Hsps) play a key role in the survival of P. falciparum in host cells. The role of the plasmodial Hsp arsenal is not limited to the protection of the parasite cell (largely through their role as molecular chaperones), as some of these proteins also promote the pathological development of malaria. This is largely due to the export of a large number of these proteins into the infected erythrocyte cytosol. Although P. falciparum erythrocyte membrane protein 1 (PfEMP1) is the main virulence factor for the malaria parasite, some of the exported plasmodial Hsps appear to augment parasite virulence. While this book largely delves into experimentally validated information on the role of Hsps in the development and pathogenicity of malaria, some of the information is based on hypotheses yet to be fully tested. Therefore, here we highlight what we know to be definite roles of plasmodial Hsps. Furthermore, we distill information that could provide practical insights on the options available for future research directions, including interventions against malaria that may target the role of Hsps in the development of the disease.

Item Type: Book Chapter
Murdoch Affiliation(s): Institute for Immunology and Infectious Diseases
Publisher: Springer, Cham
Copyright: © 2021 The Author(s), under exclusive license to Springer Nature Switzerland AG
Other Information: Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 1340)
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