ľ¹Ï¸£ÀûÓ°ÊÓ

Summary of dissertation

Respiratory viruses, such as influenza A viruses (IAVs) and coronaviruses, are a major global health concern, causing illnesses ranging from the common cold to severe, life-threatening diseases. They spread easily and pose serious risks to young children, the elderly, and those with weakened immune systems. The recent SARS-CoV-2 pandemic has underscored the importance of studying how these viruses infect us and having the best laboratory models to do so.

This thesis investigates how respiratory viruses interact with the mucus barrier and the underlying airway epithelial cells, using advanced cell culture models closely mimicking the respiratory tract, and the mucus that they produce. Mucus is our first line of defence—capturing invading virus particles and thus preventing infection. However, some viruses have means to release themselves from the molecular traps abundant throughout this layer, to reach their target airway cells. For IAV, neuraminidase is important in this respect.

Our studies show that different IAVs, depending on how they attach to cells, vary in how much they rely on their neuraminidase protein to infect cells, also in the presence of mucus. We further characterised mucus samples from different airway regions and their ability to inhibit IAV binding and infection. Lastly, we compared how well respiratory viruses replicate in different human airway models, highlighting their importance for studying recent circulating virus strains.

By increasing our understanding of how respiratory viruses bypass mucus defences and utilising the most relevant airway models, we can better predict which (animal) viruses pose a risk to infect humans and strengthen our preparedness for future outbreaks.

If a candidate gives a layman's talk, the live stream will start 15 minutes earlier.