Oxford Events, the new replacement for OxTalks, will launch on 16th March. From now until the launch of Oxford Events, new events cannot be published or edited on OxTalks while all existing records are migrated to the new platform. The existing OxTalks site will remain available to view during this period.
From 16th, Oxford Events will launch on a new website: events.ox.ac.uk, and event submissions will resume. You will need a Halo login to submit events. Full details are available on the Staff Gateway.
Chronic viral infection of the liver is a global health problem, with over 500 million individuals infected with hepatitis B (HBV) or C (HCV) viruses that cause liver disease which can progress to hepatocellular carcinoma (HCC): a metastatic cancer with limited therapeutic options. We recently discovered that low oxygen environments, naturally found in the liver, enhance HBV and HCV replication and this is mediated by hypoxia inducible transcription factors (HIFs) regulating host pathways that are essential for viral replication.
HIFs direct extensive transcriptional responses that enable a cell to respond to diverse physiological or pathophysiological signals. Hepatitis B and C viruses activate HIFs and promote a ‘pseudohypoxic’ state that potentiates viral replication. Current HCC therapies show limited efficacy and recent research efforts have focused on the molecular profiling of tumours to identify gene signatures that predict disease outcome and response to therapy. Understanding how viruses influence host gene transcription is fundamental and profiling HIF-transcriptional targets in infected cells provides a unique opportunity to define the role of HIF in viral-associated HCC heterogeneity and inform stratified approaches for new treatments.
