MAVS activation and altered T cell metabolism in atherosclerosis; Seahorse based mitochondrial metabolic studies and CRISPR/Cas-9 based gene editing.
My research interest focuses on how a triggered innate immune response to viral infections can lead to autoimmune diseases such as Systemic Lupus Erythematosus (SLE) and/or atherosclerosis. During this work I have identified that activation of the cytoplasmic, foreign RNA sensing RIG-I pathway, which is an essential innate immunity response during viral infections, can occur in absence of virus, but during oxidative stress. I have identified that the key component of the RIG-I pathway necessary for activation during oxidative stress to be the mitochondria associated antiviral protein MAVS. I have identified that MAVS oligomerization in absence of virus but under oxidative stress will lead to altered T cell metabolism as observed by Seahorse Analyzer. I have also determined the role of the MAVS prion-oligomerization on T cell proliferation and fitness. To assess the role of this protein in humans, I have founded and lead a collaborative group of investigators from Cambridge, UK, Syracuse State University and UVM to analyze a cohort of SLE patients for MAVS oligomerization in peripheral blood lymphocytes. To investigate the role of SNPs, I have pioneered at UVM the establishment of a pipeline for the genome-editing method CRISPR, which I employed successfully on cultured and primary human cells.At LCBR, I aim to expand my investigations on the role of spontaneous MAVS activation and altered T cell metabolism in atherosclerosis, with samples originating from a high number of patients.
2011 Post-Doctoral training in Immunobiology, University of Vermont2004 Ph.D., Virology, Witten/Herdecke University, Germany
2006 Post-Doctoral training in Virology, University of Vermont
1999 M.S., Biochemistry, Witten/Herdecke University, Germany
1996 B.S., Chemistry & Physics, University of Duisburg, Germany2016 - present Assistant Professor, Department of Pathology & Laboratory Medicine, University of Vermont College of Medicine, Burlington VT
2011-2016 Research Associate, Department of Medicine, University of Vermont College of Medicine, Burlington VT
2003 Konrad-Schily-Foundation Graduate Fellow
2000 Heinrich-Hertz-Foundation Fellow, Ministry of Technology and Science
2016 Massilamany C, Koenig A, Reddy J, Huber S, Buskiewicz I. Autoimmunity in picornavirus infections. Curr Opin Virol. 2016 Feb;16:8-14. PMID: 26554915
2015 Buskiewicz I, Koenig A, Massilamany C, Reddy J, Huber S. Autoimmunity in picornavirus infections. Current Opinion in Virology. 16:8-14
2015 Cunniff B, Newick K, Nelson KJ, Wozniak AN, Beuschel S, Leavitt B, Bhave A, Butnor K, Koenig A, Chouchani ET, James AM, Haynes AC, Lowther WT, Murphy MP, Shukla A, Heintz NH. Disabling Mitochondrial Peroxide Metabolism via Combinatorial Targeting of Peroxiredoxin 3 as an Effective Therapeutic Approach for Malignant Mesothelioma. PLOS One. 10(5)
2014 Koenig A, Sateriale A, Budd RC, Huber SA, Buskiewicz IA. The Role of Sex Differences in Autophagy in the Heart During Coxsackievirus B3-Induced Myocarditis. J Cardiovasc Transl Res. 7(2):182-91
2014 Koenig A, Buskiewicz IA, Fortner KA, Russell JQ, Asaoka T, He YW, Hakem R, Eriksson JE, Budd RC. The c-FLIPL cleavage product p43FLIP promotes activation of ERK, NF-?B, caspase-8 and T cell survival. J Biol Chem. 10;289(2):1183-91
2014 Buskiewicz I, Koenig A, Moussawi M, Budd RC, Huber SA. Cellular FLIPshort increases susceptibility to myocarditis from Coxsackievirus B3. PLOS One. 2014 May 9;9(5):e96156.
2012 Buskiewicz IA, Koenig A, Huber SA, Budd RC. Caspase-8 and FLIP regulate RIG-I/MDA5-induced innate immune host responses to picornaviruses. Future Virol. 2012;7(12):1221-1236.
For a complete list of Andreas Koenig's publications, please visit PubMed.