News and events Latest news & info Science on the Swan 2021 Conference Presentation Professor Ross Baker spoke on the topic of ‘WA Research Response to COVID-19’ at the Science on the Swan health and medical research conference on Monday. Held by The Western Australian Health Translation Network’s (WAHTN), the conference had a strong focus on the state’s health response to COVID-19. Prof. Baker shared PBI’s findings in relation to COVID-19 and thrombotic events, completed by himself and fellow PBI researchers, Jim Tiao and Grace Gilmore. Below is a summary of Professor Baker’s discussion at the conference. COVID-19 infection is associated with a significant risk of thrombotic events ranging from arterial embolism (blockage in an artery), acute pulmonary embolism (blockage in the lung arteries), deep vein thrombosis, microvascular (small vessel) thrombosis and stroke. It is a very common problem occurring in 1 in 4 patients with severe COVID-19 infection and it is resistant to standard treatments. Patients with COVID-19 and thrombosis have a five-fold increase in mortality and the unusual microvascular thrombosis may contribute to the reported long-term weakening and persistent symptoms in COVID-19 survivors. The development of COVID-19 related thrombosis is complex and includes many factors. It involves the interaction between the body’s normal blood clotting process and how it responds to the way its immune system reacts to the COVID-19 infection. In collaboration with an Irish COVID-19 Study looking at diseases affecting blood vessels, we have explored the imbalance between two specific components essential in the blood clotting process (von Willebrand factor (VWF) and ADAMTS-13) in COVID-19 infection. Raised levels of VWF is a risk factor for thrombosis in the veins. ADAMTS-13 circulates around the body and cuts or chops the ultra large overactive VWF and helps regulate the platelets involved in thrombus growth and blood vessel obstruction. Our research has found a five-fold increase in VWF and a severe deficiency of ADAMTS-13 in patients with COVID-19 infection, indicating a serious imbalance of this important relationship and the formation of thrombus. The signals or messages which promote an inflammatory response and prevent the function of ADAMTS-13 were also significantly elevated. We are currently examining whether the immune system develops proteins which mistakenly attack ADAMTS-13 in patients infected with COVID-19. This could lead to different therapeutic interventions, including using specific platelet-VWF inhibitors or genetically engineered ADAMTS-13, that are currently in clinical testing for treatment of rarer thrombotic disorders.