SARS-CoV-2 primarily infects lung epithelial cells. High viral replication and unbalanced immune responses can cause organ damage that may account for immediate organ failure and long-term organ dysfunction (e.g. lung fibrosis).
Similar disease manifestations are found for other respiratory viruses with pandemic potential. Here, we will characterize the pathogenic potential of SARS-CoV-2 infection and virus-specific immunity to damage lung tissue and to induce lung fibrosis.
We elucidate molecular mechanisms how virus-induced alterations of renin-angiotensin system metabolism contribute to lung fibrosis. We also investigate mechanisms, by which CD8 T cells damage different lung cells, resulting in chronic organ damage and fibrosis.
