Promotie (B.V.) Lopuhaä

Below is a brief summary of the dissertation: 

COVID-19, caused by SARS-CoV-2, can induce severe lung damage and has a higher mortality rate than other viral diseases like influenza. While many COVID-19 patients experience mild symptoms, others develop severe issues, including progressive shortness of breath, increased thrombosis, and pulmonary fibrosis. Histological examination of lung tissue reveals diffuse alveolar damage, with an overactive immune response believed to contribute to this damage, though the exact mechanisms remain unclear.
Through protein and gene expression analysis of post-mortem lung tissue from SARS-CoV-2-infected patients, this thesis highlights a significant increase in mast cell activity compared to influenza patients, which may contribute to pulmonary fibrosis and thrombosis. Further investigation of protein expression in isolated pulmonary thrombi reveals an increase in platelet-derived proteins. Since venous blood clots typically contain more platelets than arterial clots, this suggests that venous thrombosis plays a more prominent role in COVID-19 compared to arterial thrombosis.
Comparing histological findings from humans and minks infected with SARS-CoV-2, both species exhibit similar tissue changes, though pulmonary thrombi and fibrosis are more prominent in humans. Protome of lung tissue in both species shows increased pathways related to inflammation, blood coagulation, and lung fibrosis, indicating a similar response to the virus despite differences in histological evidence.
Lastly, pathology reports from COVID-19 autopsies in the Netherlands reveal varying lung damage severity across pandemic waves, with more thrombi and alveolar damage in earlier waves. Through automated registration and standardized coding, this registry allows for monitoring long-term effects of COVID-19.
Ultimately, this thesis provides valuable insights into the pathophysiology of COVID-19.