fig1

Earliest hepatitis B virus-hepatocyte genome integration: sites, mechanism, and significance in carcinogenesis

Figure 1. Schematic presentation of the detection and evolution of markers of virus infection and its genomic integration, hepatocyte DNA damage, and indicators of hepatocyte oxidative stress and activity of DNA repair machinery in the first 72 h after contact with infectious HBV or WHV. The graphs are based on combined results from HBV and WHV infections in hepatocyte-compatible cells and from woodchucks experimentally infected with wild-type WHV, as detailed in the text. Star on bar represents the time at which peak expression or activity was observed. HBV: hepatitis B virus; WHV: woodchuck hepatitis virus; ROS: reactive oxygen species; RNS: reactive nitrogen species; HO1: heme oxygenase-1; PARP1: poly(ADP-ribose) polymerase 1; XRCC1: X-ray repair cross-complementing protein 1; NAD+: nicotinamine adenine dinucleotide; OGG1: 8-oxyguanidine DNA glucose 1; nt: not tested beyond the time point indicated.

Hepatoma Research
ISSN 2454-2520 (Online) 2394-5079 (Print)

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