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- W2912591356 abstract "Hepatitis B virus (HBV) is one of the world’s unconquered diseases, with 370 million chronically infected globally. HBV replicates in hepatocytes within the liver that exist under a range of oxygen tensions from 11% in the peri-portal area to 3% in the peri-central lobules. HBV transgenic mice show a zonal pattern of' viral antigen with expression in the peri-central areas supporting a hypothesis that low oxygen regulates HBV replication. We investigated this hypothesis using a recently developed in vitro model system that supports HBV replication. We demonstrate that low oxygen significantly increases covalently closed circular viral DNA (cccDNA), viral promoter activity and pre-genomic RNA (pgRNA) level, consistent with low oxygen boosting viral transcription. Hypoxia inducible factors (HIFs) regulate cellular responses to low oxygen and we investigated a role for HIF-1(alpha) or HIF-2(alpha) on viral transcription. A combination of HIF inhibitors and silencing of HIF-l(alpha) and HIF-2(alpha) ablated the effect of low oxygen on cccDNA and pgRNA, suggesting a role in regulating HBV transcription. This study highlights a new role for hepatic oxygen levels to regulate multiple steps in the HBV life cycle and this may impact on future treatments for viral associated pathologies." @default.
- W2912591356 created "2019-02-21" @default.
- W2912591356 creator A5088689955 @default.
- W2912591356 date "2018-07-01" @default.
- W2912591356 modified "2023-09-23" @default.
- W2912591356 title "Impact of hypoxia on hepatitis B virus replication" @default.
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