Detail

Keywords

Host-Pathogen Interactions; Inflammation; Metabolism; Molecular Medicine; Pathology; Systems Biology; T Cells; Virology

Research group(s)

• Bergthaler Lab
  Research Area: Infection Biology, Inflammation, Metabolism, Virology, Pathology, Evolution, Systems Biology
  Members:
  Andreas Bergthaler

Research interests

The aims of my research group are to tackle the inherently complex dynamics of host-pathogen interactions through a systemic and inclusive perspective on disease-relevant molecular mechanisms. We employ integrative approaches of immunology, virology, genetics, evolution, metabolomics, pathology and systems biology for fundamental questions of infectious diseases and inflammation. We are intrigued about structural and communication features of tissues within the organism, their different responses to viral infections and the role of intracellular and systemic metabolism. A particular focus of us rests on parenchymal cells and their interactions with immune cells and distal organs. We consider time kinetics as a central dimension for a better understanding of host-pathogen interactions and are interested in the evolutionary dynamics of how viruses evade the selection pressure of antiviral immune responses. We pursue cross-disciplinary research within our diverse and international team and through collaborations with leaders in their respective field. We recognize that many of the aforementioned features of infections may have functional counterparts in other inflammatory diseases including cancer and autoimmunity. We, thus, expect that a better mechanistic understanding of the molecular processes of viral pathogenesis may help to pave the way for novel therapeutic avenues in infectious and sterile inflammatory diseases.

Selected publications

1. Lercher, A. et al., 2019. Type I Interferon Signaling Disrupts the Hepatic Urea Cycle and Alters Systemic Metabolism to Suppress T Cell Function. Immunity, 51(6), pp.1074–1087.e9. Available at: http://dx.doi.org/10.1016/j.immuni.2019.10.014.
2. Baazim, H. et al., 2019. CD8+ T cells induce cachexia during chronic viral infection. Nature Immunology, 20(6), pp.701–710. Available at: http://dx.doi.org/10.1038/s41590-019-0397-y.
3. Kosack, L. et al., 2019. The ERBB-STAT3 Axis Drives Tasmanian Devil Facial Tumor Disease. Cancer Cell, 35(1), pp.125–139.e9. Available at: http://dx.doi.org/10.1016/j.ccell.2018.11.018.
4. Bhattacharya, A. et al., 2015. Superoxide Dismutase 1 Protects Hepatocytes from Type I Interferon-Driven Oxidative Damage. Immunity, 43(5), pp.974–986. Available at: http://dx.doi.org/10.1016/j.immuni.2015.10.013.
5. Schliehe, C. et al., 2014. The methyltransferase Setdb2 mediates virus-induced susceptibility to bacterial superinfection. Nature Immunology, 16(1), pp.67–74. Available at: http://dx.doi.org/10.1038/ni.3046.