Andreas Bergthaler

Our group explores how inflammatory processes are regulated and how the immune system responds to viral infections. Using well-defined mouse infection models and cell culture systems, combined with molecular techniques from immunology, virology, and systems biology, we aim to gain insights into viral pathogenesis and the antiviral immune response. Our ultimate goal is to understand pathogen control and tissue damage development to identify new therapeutic approaches for infectious and inflammatory diseases.

Systemic Crosstalk Between Metabolism and Inflammation

Inflammatory processes are closely linked to metabolic pathways, including secreted metabolites and cytokines. However, the metabolic-inflammatory crosstalk at the organism level is not well understood. Our research focuses on characterizing these processes using models of acute and chronic viral infections. The liver, as a central organ for metabolism, is a key focus due to its role in processing and distributing signals. By integrating systems-level and hypothesis-driven approaches, we aim to identify regulatory nodes between metabolism and inflammation.

Interplay Between Persistent Viruses and the Host Immune System

Persistent viral infections affect millions globally, yet treatment options are limited due to a lack of understanding of the viruses' molecular mechanisms. Using the lymphocytic choriomeningitis virus as a model, we study how viruses interact with the immune system and sustain infections. Our research focuses on the antiviral innate immune response, organ-specific CD8 T cell responses, and viral evasion strategies during chronic infection.

Pathogenesis of Virus-Induced Immunopathologies

Viral infections often lead to severe co-morbidities such as hepatitis or pneumonia. These infections can suppress the immune system, facilitating superinfections by bacteria or other viruses. We investigate the molecular interactions between pathogens and their hosts in various infection models, including influenza virus. Our goal is to identify critical disease-driving processes and molecules for targeted therapeutic interventions.

Molecular Basis of Transmissible Cancers

Transmissible cancers are rare but occur in animals like dogs, mollusks, and Tasmanian devils. These cancers provide insights into the intersection of cancer and infectious diseases. We study the devil facial tumor disease (DFTD) in Tasmanian devils, focusing on the mechanisms driving cancer growth and immune evasion. Our research also explores pharmacological targeting of DFTD to support conservation efforts for Tasmanian devils.

Andreas Bergthaler studied veterinary medicine at the University of Veterinary Medicine in Vienna. For his graduate studies, he joined the Institute of Experimental Immunology at the ETH and University of Zurich (Professors Hans Hengartner and Nobel laureate Rolf Zinkernagel). After postdoctoral work in the laboratory of Professor Daniel Pinschewer at the University of Geneva, he worked with Professor Alan Aderem at the Institute for Systems Biology in Seattle. From 2011 to 2021, Andreas Bergthaler developed his own independent research group as CeMM principal investigator. In January 2022, he became professor of molecular immunology at MedUni Vienna and remains CeMM adjunct principal investigator. The Bergthaler laboratory pursues two main research directions: 1) Dissection of the molecular interplay of inflammation and metabolism on an organismal level. Here, a particular focus rests on the enigmatic multi-organ disease cachexia, which affects many patients suffering from chronic infections, terminal cancer, or autoinflammatory diseases. 2) Development of advanced pathogen surveillance on the population level. To this end, new approaches and analytic tools are developed to detect pathogens in wastewater and air filters and to inform public health decisions. Andreas Bergthaler is the recipient of an ERC Starting Grant and several awards including the Loffler-Frosch-Prize of the Society of Virology. He cofounded several companies including the clinical stage company Hookipa Pharma, which develops immunotherapies for infectious and malignant diseases.

Amman F, Markt R, et al. Viral variant-resolved wastewater surveillance of SARS-CoV-2 at national scale. Nat Biotech. 2022 Dec;40(12):1814-1822. (abstract)

Baazim H et al. The interplay of immunology and cachexia in infection and cancer. Nat Rev Immunol. 2022 May;22(5):309-321. (abstract)

Agerer B et al. SARS-CoV-2 mutations in MHC-I-restricted epitopes evade CD8+ T-cell responses. Sci Immunol. 2021 Mar 4;6(57):eabg6461. (abstract)

Popa A et al. Genomic epidemiology of superspreading events in Austria reveals mutational dynamics and transmission properties of SARS-CoV-2. Sci Transl Med. 2020 Dec 9;12(573):eabe2555. (abstract)

Lercher A et al. Systemic Immunometabolism: Challenges and Opportunities. Immunity. 2020 Sep 15;53(3):496-509. (abstract)

Lercher A*, Bhattacharya A* et al. Type I interferon signaling disrupts the hepatic urea cycle and alters systemic metabolism to suppress T-cell function. Immunity. 2019 Dec 17;51(6):1074-1087.e9. (abstract)

Baazim H et al. CD8(+) T-cells induce cachexia during chronic viral infection. Nat Immunol. 2019 Jun;20(6):701-710. (abstract)

Kosack L*, Wingelhofer B*, Popa A*, Orlova A* et al. The ERBB-STAT3 Axis Drives Tasmanian Devil Facial Tumor Disease. Cancer Cell. 2019 Jan 14;35(1):125-139.e9. (abstract)

Khamina K , et al. Characterization of host proteins interacting with the lymphocytic choriomeningitis virus L protein. PLoS Pathog. 2017 Dec 20;13(12):e1006758. (abstract)

Bhattacharya A, et al. Superoxide dismutase 1 protects from type I interferon-driven oxidative damage in viral hepatitis. Immunity. 2015 Nov 17;43(5):974-86. (abstract)

Schliehe C. et al. The methyltransferase Setdb2 mediates virus-induced susceptibility to bacterial superinfection. Nat Immunol. 2015 Jan;16(1):67-74. (abstract)

Johnson S, et al. Protective Efficacy of Individual CD8+ T Cell Specificities in Chronic Viral Infection. J Immunol. 2015 Feb 15; 194(4):1755-62. (abstract)

Schliehe C. et al. The methyltransferase Setdb2 mediates virus-induced susceptibility to bacterial superinfection. Nat Immunol. 2015 Jan;16(1):67-74. (abstract)

Litvak V, et al. A FOXO3-IRF7 gene regulatory circuit limits inflammatory sequelae of antiviral  responses. Nature 2012 Oct 18; 490(7420):421-5. doi: 10.1038/nature11428. Epub 2012 Sep 16. (abstract)

Bergthaler A, et al. Viral replicative capacity is the primary determinant of lymphocytic choriomeningitis virus persistence and immunosuppression. Proc Natl Acad Sci U S A. 2010 Dec 14;107(50):21641-6. (abstract)

Hegazy AN, et al. Interferons direct Th2 cell reprogramming to generate a stable GATA-3(+)T-bet(+) cell subset with combined Th2 and Th1 cell functions. Immunity. 2010 Jan 29;32(1):116-28. (abstract)

Bergthaler A, et al. Impaired antibody response causes persistence of prototypic T cell-contained virus. PLoS Biol. 2009 Apr 7;7(4):e1000080. (abstract)