Innovative Liver Disease Models and HBV
The Michailidis laboratory is interested in understanding the molecular and cellular mechanisms that drive virus-host interactions, how viruses lead to human diseases, and the strategies we can develop to control them. In particular, we are interested in hepatitis B virus (HBV), its target cells, the hepatocytes, and the crosstalk between innate immunity and metabolism in the liver. With physiologically relevant in vitro and in vivo systems and state-of-the-art technologies ranging from single-cell transcriptomics to whole-genome CRISPR editing, there is a great potential to uncover the mechanisms that govern chronic hepatitis B and ultimately cure this deadly disease. Furthermore, using similar strategies we want to extend our knowledge across multidisciplinary fields, including other hepatotropic infections, liver-related diseases and liver functions.
Innate Immune Responses and ISGs
The innate immune response, driven by interferon (IFN), protects cells against invading viral pathogens. The workhorses that mediate this defense are the products of hundreds of IFN-stimulated genes (ISGs). Our previous work with HBV, Zika virus and multiple coronaviruses, including SARS-CoV-2, has revealed a set of ISGs that have a drastic effect on viral replication. Our objective is to characterize the mechanism of action of these ISGs and inform the development of new antiviral strategies. Towards this goal we employ a diverse set of molecular, cellular, and biochemical tools.
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