Please use this identifier to cite or link to this item: https://doi.org/10.3390/v13030524
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dc.titleLiver-Derived Cell Transfection Model Efficacy for HBV Genotype B Replication/Transcription Is Determined by Complex Host Transcription Factor Network
dc.contributor.authorChong, Roxanne Hui-Heng
dc.contributor.authorKhakpoor, Atefeh
dc.contributor.authorTan, Theresa May-Chin
dc.contributor.authorLim, Seng-Gee
dc.contributor.authorLee, Guan-Huei
dc.date.accessioned2021-11-16T07:34:00Z
dc.date.available2021-11-16T07:34:00Z
dc.date.issued2021-03-01
dc.identifier.citationChong, Roxanne Hui-Heng, Khakpoor, Atefeh, Tan, Theresa May-Chin, Lim, Seng-Gee, Lee, Guan-Huei (2021-03-01). Liver-Derived Cell Transfection Model Efficacy for HBV Genotype B Replication/Transcription Is Determined by Complex Host Transcription Factor Network. VIRUSES-BASEL 13 (3). ScholarBank@NUS Repository. https://doi.org/10.3390/v13030524
dc.identifier.issn19994915
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/206420
dc.description.abstractBackground: Interaction between host transcription factors (TFs) and the viral genome is fundamental for hepatitis B virus (HBV) gene expression regulation. Additionally, the distinct interaction of the TFs’ network with the HBV genome determines the regulatory effect outcome. Hence, different HBV genotypes and their variants may display different viral replication/transcription reg-ulation. Due to the lack of an efficient infection model suitable for all HBV genotypes, the hepatoma cell transfection model is primarily used in studies involving non-D HBV genotypes and variants. Methods: We explored the transcriptome profile of host TFs with a regulatory effect on HBV in eight liver-derived cell lines in comparison with primary human hepatocytes (PHH). We further analyzed the suitability of these models in supporting HBV genotype B replication/transcription. Results: Among studied models, HC-04, as a result of the close similarity of TFs transcriptome profile to PHH and the interaction of specific TFs including HNF4α and PPARα, showed the highest efficiency in regard to viral replication and antigen production. The absence of TFs expression in L02 transfection model resulted in its inefficiency in HBV replication/transcription. Conclusion: These observations help to better design studies on regulatory mechanisms involving non-D HBV genotypes and variants’ gene expression and the development of more efficient therapeutical approaches.
dc.language.isoen
dc.publisherMDPI
dc.sourceElements
dc.subjectScience & Technology
dc.subjectLife Sciences & Biomedicine
dc.subjectVirology
dc.subjecthepatitis B virus
dc.subjecttranscription factor
dc.subjecttransfection model
dc.subjectgenotype B
dc.typeArticle
dc.date.updated2021-11-10T14:19:35Z
dc.contributor.departmentDUKE-NUS MEDICAL SCHOOL
dc.contributor.departmentBIOCHEMISTRY
dc.contributor.departmentMEDICINE
dc.description.doi10.3390/v13030524
dc.description.sourcetitleVIRUSES-BASEL
dc.description.volume13
dc.description.issue3
dc.published.statePublished
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