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The role of an expanded family of exported effector kinases in environmental sensing and regulation of virulence in human malaria.

Project description

A closer look at FIKK kinases in malaria parasites

Malaria is a life-threatening infection. Its most severe form is caused by the protozoan parasite Plasmodium falciparum. The main contributors are cytoadhesion of infected red blood cells (iRBC) to host endothelium, and iRBC rigidification obstructing iRBC clearance in the spleen and promoting parasite survival. The parasite has to balance between preventing its own clearance through sufficiently strong cytoadhesion and control of rigidity and killing the host. Strong evidence indicates that the parasite can rapidly regulate its cytopathy properties through the FIKK kinases, making it important to understand FIKK function. The EU-funded VirulenceControl project will apply advanced approaches to identify the role of FIKK kinases and their molecular underpinnings in controlling cytoadhesion and rigidity in conditions frequently found in the human host.

Objective

The most severe form of malaria in humans is caused by Plasmodium falciparum. Cytoadhesion of infected red blood cells (iRBCs) to host endothelium and iRBC rigidification are the major contributors to pathology. Cytoadhesion is mediated by transport of a protein called PfEMP1 onto the surface of the iRBC. It prevents clearance of iRBCs in the spleen and promotes parasite survival, but can cause the obstruction of blood vessels leading to pathology. Thus, the parasite has to strike a fine balance between preventing its own clearance through sufficiently strong cytoadhesion and control of rigidity, and killing the host. The paradigm in the field is that the strength of cytoadhesion is dominated by expression of PfEMP1 variants with different affinities for host cell receptors. We now have strong evidence that the parasite can rapidly regulate its cytoadhesive properties using a family of atypical kinases (the FIKK kinases) it exports into the host cell. This gives the parasite a yet unrecognized ability to respond to conditions encountered in the host, such as fever or hypoxia in areas of high parasite sequestration, and influence disease outcome. This is important: Of the 6 human infecting Plasmodium species only P. falciparum exports FIKK kinases into the host cell. As this species is responsible for ~95% of all fatal human malaria cases, it is paramount to understand FIKK- function in pathogenesis. We will use cutting edge approaches to: (1) identify the function of FIKK kinases in controlling cytoadhesion and rigidity in conditions frequently encountered in the human host and determine RBC remodelling in samples from patients. (2) Identify the molecular underpinnings of FIKK function in controlling cytoadhesion and (3) perform a thorough biochemical characterisation of the atypical FIKK kinase family. In summary we aim to answer the paramount question about the functional role and the evolution of the FIKK kinases and the pathogenesis of P. falciparum malaria.

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HORIZON-ERC - HORIZON ERC Grants

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Call for proposal

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(opens in new window) ERC-2021-COG

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Host institution

FUNDACAO GIMM - GULBENKIAN INSTITUTE FOR MOLECULAR MEDICINE
Net EU contribution

Net EU financial contribution. The sum of money that the participant receives, deducted by the EU contribution to its linked third party. It considers the distribution of the EU financial contribution between direct beneficiaries of the project and other types of participants, like third-party participants.

€ 1 796 073,00
Address
AVENIDA PROFESSOR EGAS MONIZ
1649-035 LISBOA
Portugal

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Total cost

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€ 1 796 073,00

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