Academic Rank:
Clinical Professor, Pathology and Laboratory Medicine, UBC
Scientist, Canadian Blood Services
Short Bio:

Current Positions

  • Scientist, Canadian Blood Services
  • Clinical Professor, Pathology and Laboratory Medicine
  • Associate Director, Centre for Blood Research

Dr. Pryzdial obtained his Ph.D. at the University of Toronto in biochemistry, with postdoctoral training at the National Institutes of Health, Center of Excellence in Thrombosis at the University of Vermont.  He is now a Scientist at the Canadian Blood Services, Centre for Innovation, and Associate Director at the University of  British Columbia, Centre for Blood Research ( where he holds a faculty position as Clinical Professor in the Department of Pathology and Laboratory Medicine. Among other affiliations, Ed Chairs a scientific advisory sub-committee for the Heart and Stroke Foundation of Canada, is a member of the Scientific Advisory Committee for the Canadian HemophiliaSociety and is an Editorial Advisory Board member for the Biochemical Journal. The work in his laboratory focuses on clotting  protein biochemistry in fibrinolysis, virology and rare coagulation disorders. The work in has lab is currently funded by the Canadian Institutes of Health Research, the Heart and Stroke Foundation of Canada and BiogenIdec.

Academic background

  • PhD, University of Toronto, Biochemistry. 1987
  • BSc, University of Toronto, Biology (Major), Chemistry (Minor), Biochemistry, Specialist. 1981

Dr. Pryzdial’s doctoral work was on the physical biochemistry of complement protein interactions at the University of Toronto. Although staying in blood protein research, postdoctoral training at the NIH Specialized Centre of Research in Thrombosis, University of Vermont shifted his interests to blood clotting biochemistry. Joining Canadian Blood Services (at that time part of the Red Cross Society) and University of Ottawa in 1990/91, he transferred his laboratory in 2001 to become a member of the UBC Centre for Blood Research. Dr. Pryzdial’s lab members investigate: the regulation of clot formation and how it dissolves; how viruses exploit blood proteins to enhance cellular infection; and the molecular basis of patients with clotting protein deficiency. Particular emphasis is placed on novel applications of plasma proteins to transfusion science and advancing our understanding of heart disease. (,

Research Interest

  • Blood Proteins
  • Coagulation and Fibrinolysis
  • Role of Blood Proteins in Viral Infection

The general expertise in our laboratory is the function of blood proteins and there novel application. By combining biochemistry and molecular engineering, we have discovered new functions of several proteins with possible therapeutic or diagnostic applications to heart disease and virus infection. Our long-range goal is to understand how these findings may impact on other blood protein functions and thereby contribute to optimizing the value derived from blood constituents and their substitutes.

Communication Between Clot-Forming and Clot-Dissolving Proteins

Clot generation (coagulation) and subsequent clearance (fibrinolysis) are fundamental biological processes. A high degree of communication between these opposing pathways is necessary to ensure that clots form and dissolve sequentially, and only when needed. The biological effector of coagulation, thrombin, is activated by an enzyme complex consisting of the protease factor Xa (FXa) and its cofactor Va (FVa). In recent work, Dr. Pryzdial’s group identified a previously unknown mechanism of communication between these clotting factors and the fibrinolysis pathway. The data revealed that FXa and FVa accelerate the clot-buster, tissue plasminogen activator (tPA), which is used as an important therapeutic. These studies suggest that the current fibrinolysis dogma must be revised to include auxiliary tPA cofactors, such as FXa and FVa, in the vicinity of the clot to further understand vascular health and pathology.

Blood Proteins Exploited by Viruses

For decades many viruses have been linked to heart disease. To understand the molecular basis of the clinical correlation, Dr. Pryzdial’s group found that at least herpes simplex virus type 1 and type 2, and cytomegalovirus can directly assemble clotting protein complexes on their surfaces to generate thrombin. This bypasses the normally strict regulation of coagulation imposed by cells. Virus initiated clot formation not only contributes to heart disease, but enhances the susceptibility of host cell infection through protease activated receptors and possibly annexins. Dr. Pryzdial and his lab members are further dissecting the specific host- and virus-derived proteins on the virus surface that trigger coagulation and their role in virus propagation.