Publications by authors named "Laura Meiss-Heydmann"
Article Synopsis
- Chronic HBV infection leads to severe liver disease and liver cancer, and new antiviral treatments like Capsid Assembly Modulators (CAMs) are needed but not fully understood in their mechanism of action.
- Recent research demonstrates that CAM-A compounds reduce HBsAg levels and cause cell death in HBV-infected cells by promoting the aggregation of HBV core proteins (HBc) in the nucleus, triggering apoptosis.
- Discovering that CAM-A facilitates HBc aggregation and activates apoptosis provides insights for developing new therapies aimed at effectively managing chronic HBV infections.
Background & Aims: Liver fibrosis is the major driver of hepatocellular carcinoma and liver disease-related death. Approved antifibrotic therapies are absent and compounds in development have limited efficacy. Increased TGF-β signaling drives collagen deposition by hepatic stellate cells (HSCs)/myofibroblasts.
View Article and Find Full Text PDFBackground & Aims: Chronic co-infection with HBV and HDV leads to the most aggressive form of chronic viral hepatitis. To date, no treatment induces efficient viral clearance, and a better characterization of virus-host interactions is required to develop new therapeutic strategies.
Methods: Using loss-of-function strategies, we validated the unexpected proviral activity of Janus kinase 1 (JAK1) - a key player in innate immunity - in the HDV life cycle and determined its mechanism of action on HDV through various functional analyses including co-immunoprecipitation assays.