Investigating the Immune Mechanisms Underlying the Development of Rheumatological Complications Post-COVID

The coronavirus pandemic has severely affected global healthcare systems and changed life as we know it. It is now apparent that beyond the resolution of infection, a subset of COVID-19 patients who recover sustain a range of persistent symptoms ranging from chronic fatigue, shortness of breath and joint pain to cognitive impairments and cardiovascular complications. This constellation of symptoms is known together as post-acute COVID-19 sequelae (PACS) or long-COVID. Persistent autoantibodies post-COVID are well documented 3 months, 6 months, and 12 months following infection indicating that the inappropriate activation of the immune system and the development of autoimmune responses plays a role in continued symptomology post infection. Furthermore, these changes in the immune system may lead to the development of chronic and serious rheumatic diseases like lupus, rheumatoid arthritis, vasculitis, scleroderma, and others. My Master's thesis aims to understand the precise mechanisms of immune system impairment which initiates autoimmunity, describe the B-cell populations which may mediate auto-antibody formation, and describe how the post-COVID condition is influenced by aberrant neutrophil activation and coagulation dysfunction. A thorough understanding of these mechanisms will assist in identifying early biomarkers of disease and establish a path to possible treatment avenues and therapeutic interventions.