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| Status |
Public on Oct 01, 2019 |
| Title |
Molecular signature of hepatitis B virus regulation by IFN-γ in primary human hepatocyte |
| Organism |
Homo sapiens |
| Experiment type |
Expression profiling by array
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| Summary |
Hepatitis B virus (HBV) infection is a risk of developing fibrosis, cirrhosis, liver failure, and hepatocellular carcinoma. Although HBV elimination requires complete elimination of covalently closed circular DNA (cccDNA), its treatment has not been established. Interferon (IFN) -γ, a type ⅠⅠ IFN, is produced by intrahepatic cytotoxic T lymphocytes and has the noncytolytic antiviral potential. However, the mechanism by which IFN-γ regulates HBV infection in hepatocytes has not been fully elucidated. In this study, to replicate the HBV infection and monitor the amount of cccDNA, we developed an in vitro HBV infection assay system with primary hepatocytes and examined the molecules and signaling pathways. IFN-γ suppressed both HBV propagation and transcription to the same extent as IFN-α. RNA microarray analysis revealed that IFN-γ stimulation induced not only IFN-γ but also IFN-α signaling activation and regulated HBV cccDNA. Moreover, the HBV production was reduced by IFN-γ through JAK-STAT signaling and interferon stimulated genes such as OAS2 and APOBEC3G. Taken together, these results demonstrate that IFN-γ suppresses both HBV propagation and transcription by activating specific intracellular signaling pathways in hepatocytes and suggests the future application of this particular signaling pathways or genes for the complete elimination of HBV.
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| Overall design |
The comprehensive gene expression profiles were investigated in the primary human hepatocytes derived from chimeric mice with human liver (PXB cells). PXB cells were infected with HBV at Day 0 and IFN-γ or IFN-α was added to each medium from day 4 after the infection. PXB cells were harvested at 22 days after the infection. The comparison combinations used in this analysis were the ratios Control/ IFN-γ or Control/ IFN-α.
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| Contributor(s) |
Nosaka T, Naito T, Matsuda H, Hiramatsu K, Ohtani M, Nemoto T, Nishizawa T, Okamoto H, Nakamoto Y |
| Citation(s) |
31733138 |
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| Submission date |
Jun 12, 2019 |
| Last update date |
Jan 03, 2020 |
| Contact name |
Takuto Nosaka |
| E-mail(s) |
nosat@u-fukui.ac.jp
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| Phone |
+81-776-61-8351
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| Organization name |
University of Fukui
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| Department |
Second Department of Internal Medicine
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| Street address |
23-3 Matsuoka, Eiheiji-cho
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| City |
Yoshida-gun |
| State/province |
Fukui |
| ZIP/Postal code |
910-1193 |
| Country |
Japan |
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| Platforms (1) |
| GPL20844 |
Agilent-072363 SurePrint G3 Human GE v3 8x60K Microarray 039494 [Feature Number Version] |
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| Samples (4)
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| Relations |
| BioProject |
PRJNA548541 |
| Supplementary file |
Size |
Download |
File type/resource |
| GSE132628_Matrix_table.xlsx |
2.6 Mb |
(ftp)(http) |
XLSX |
| GSE132628_RAW.tar |
22.2 Mb |
(http)(custom) |
TAR (of TXT) |
| Processed data included within Sample table |
| Processed data are available on Series record |
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