The role of von Willebrand Factor (VWF) in malaria pathogenesis. (360G-Wellcome-081345_Z_06_Z)

The pathogenicity of Plasmodium falciparum is thought to relate to the unique ability of infected erythrocytes to adhere to and subsequently activate the vascular endothelium. The primary process of cytoadherence has been studied in detail and a large number of receptors have been identified as being able to mediate binding of infected erythrocytes (IE). Host endothelia have differential receptor expression, for example cerebral endothelium has little or no CD36 which could influence parasite sequestration, limiting it to IE able to bind to other receptors. Recently however sequestration of IE to brain endothelium by CD36-binding variants has been demonstrated in paediatric cerebral malaria through bridging by platelets. Our recent work has shown that levels of von Willebrand factor (VWF) and its pro-peptide are elevated in malaria, indicating fulminant and specific endothelial activation and providing a mechanism for platelet accumulation on endothelium. The aims of this study ar e; i) To confirm the increased regulated expression of VWF in malaria. ii) To elucidate its potential role in the platelet bridging adhesion mechanism, including VWF multimerisation and proteolytic turnover. iii) To investigate the molecular mechanisms of VWF-mediated cytoadherence. iv) To examine its significance in paediatric disease.

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Grant Details

Amount Awarded 307716
Applicant Surname Craig
Approval Committee Tropical and Clinical Immunology and Infectious Disease Funding Committee
Award Date 2006-10-16T00:00:00+00:00
Financial Year 2006/07
Grant Programme: Title Project funding: Inactive scheme
Internal ID 081345/Z/06/Z
Lead Applicant Prof Alister Craig
Other Applicant(s) Dr Georges Grau, Dr James Bunn, Prof James O'Donnell, Prof Jan Van Mourik
Partnership Value 307716
Planned Dates: End Date 2010-07-31T00:00:00+00:00
Planned Dates: Start Date 2007-01-01T00:00:00+00:00
Recipient Org: Country United Kingdom
Region North West