Type I interferon signaling and mitochondrial dysfunction in the heart in acute and long/post COVID disease
Project leader: Dr. Georgios Amanakis
Research field
- Basic and translational research on post COVID
Who is involved?
- Dr. Georgios Amanakis (Project leader, MHH)
- Prof. Dr. Ulrich Kalinke (TWINCORE)
- Prof. Dr. Asisa Volz (TiHo)
- Prof. Dr. Maren von Köckritz-Blickwede (TiHo)
- Prof. Dr. Wolfgang Baumgärtner (TiHo)
What is the aim?
Although the long/post COVID syndrome poses significant challenges to the German healthcare system, its pathophysiology is not yet understood. A subset of reported symptoms may be attributed to the heart, however, the effects of SARS-CoV-2 in the heart are largely unclear. There is a critical need to study the cardiac pathophysiology of SARS-CoV-2. Without this knowledge, diagnosis and treatment of long/post COVID will remain difficult.
The long-term goal of this study is to identify potential therapeutic targets for acute and long/post COVID. The central hypothesis is that cardiac mitochondria play a role in regulating interferon signaling and in the pathogenesis of the symptoms. In this context, the specific aims are:
- To identify key regulators of type I interferon signaling in the myocardium in acute and long COVID.
- To determine myocardial mitochondrial dysfunction and redox imbalance in acute and long/post COVID.
- To characterize myocardial cell death and microscopic changes in acute and long/post COVID.
To validate our hypothesis, we will use the COFONI mouse technology platform. Mice will be infected with a mouse-adapted SARS-CoV-2 strain, closely resembling the phenotype observed in humans. The expected outcome of this research is to elicit how interferon signaling regulates the permissiveness of the heart tissue to virus infection and how mitochondrial function is affected by the infection and might result in downstream microscopic changes of the myocardium. These outcomes are expected to serve as the basis for the development of new treatment options.