Viral infection by Hepatitis B virus (HBV) causes many hepatocyte changes due to the direct action of a protein encoded by the virus, HBx, and to indirect changes due to a large increase in intracellular reactive oxygen species (ROS) after infection. HBx appears to dysregulate a number of cellular pathways. HBx causes dysregulation in part by binding to genomic DNA, changing expression patterns of miRNAs, affecting histone methyltransferases, binding to SIRT1 protein to activate transcription, and cooperating with histone methylases and demethylases to change cell expression patterns. HBx is partly responsible for the approximate 10,000-fold increase in intracellular ROS upon chronic HBV infection. Increased ROS can be caused, in part, by localization of HBx to the mitochondria where HBx decreases the mitochondrial membrane potential.
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