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Modeling Hepatitis B Virus Infection in Non-Hepatic 293T-NE-3NRs Cells
Published on: June 5, 2020
Effect of oxidative stress and calcium deregulation on FAM26F (CALHM6) expression during hepatitis B virus infection
Kehkshan Jabeen1, Uzma Malik2, Sajid Mansoor2,3
1Genomics Research Lab, Department of Biological Sciences, International Islamic University Islamabad, Islamabad, 44000, Pakistan.
Background:
Family with sequence similarity 26, member F (FAM26F) is an important innate immunity modulator playing a significant role in diverse immune responses, however, the association of FAM26F expression with HBV infection is not yet known. Thus, the current study aims to explore the differential expression of FAM26F in vitro in HepAD38 and HepG2 cell lines upon HBV infection, and in vivo in HBV infected individuals. The effects of antioxidant and calcium inhibitors on the regulation of FAM26F expression were also evaluated. The expression of FAM26F was simultaneously determined with well-established HBV infection markers: IRF3, and IFN-β.
Methods:
The expression of FAM26F and marker genes was analyzed through Real-time qPCR and western blot.
Results:
Our results indicate that the differential expression of FAM26F followed the same trend as that of IRF3 and IFN-β. The in vitro study revealed that, in both HBV infected cell lines, FAM26F expression was significantly down-regulated as compared to uninfected control cells. Treatment of cells with N-acetyl-L-cysteine (NAC), EGTA-AM, BAPTA-AM, and Ru360 significantly upregulated the expression of FAM26F in both the cell lines. Moreover, in in vivo study, FAM26F expression was significantly downregulated in all HBV infected groups as compared to controls (p = 0.0007). The expression was higher in the HBV recovered cases, probably due to the decrease in infection and increase in the immunity of these individuals.
Conclusion:
Our study is the first to show the association of FAM26F with HBV infection. It is proposed that FAM26F expression could be an early predictive marker for HBV infection, and thus is worthy of further investigation.
Insights
Family with sequence similarity 26, member F (FAM26F) expression is significantly down-regulated during Hepatitis B Virus (HBV) infection. This study suggests FAM26F may serve as an early predictive marker for HBV infection.
Area of Science:
- Immunology
- Hepatology
- Molecular Biology
Background:
- Family with sequence similarity 26, member F (FAM26F) is a key innate immunity modulator.
- The role of FAM26F in Hepatitis B Virus (HBV) infection remains uncharacterized.
- Investigating FAM26F's role in HBV infection is crucial for understanding immune responses.
Purpose of the Study:
- To explore the differential expression of FAM26F in HBV-infected cell lines and individuals.
- To evaluate the effects of antioxidants and calcium inhibitors on FAM26F regulation.
- To correlate FAM26F expression with established HBV infection markers like IRF3 and IFN-β.
Main Methods:
- Real-time quantitative polymerase chain reaction (qPCR) for gene expression analysis.
- Western blot assays to assess protein levels.
- In vitro studies using HepAD38 and HepG2 cell lines, and in vivo studies with HBV-infected individuals.
Main Results:
- FAM26F expression mirrored the trends of IRF3 and IFN-β, key HBV infection markers.
- FAM26F was significantly downregulated in HBV-infected cell lines and individuals compared to controls.
- Antioxidants (NAC) and calcium inhibitors (EGTA-AM, BAPTA-AM, Ru360) upregulated FAM26F expression.
- Higher FAM26F expression was observed in recovered HBV cases, indicating a potential immune recovery marker.
Conclusions:
- This is the first study to establish a link between FAM26F and HBV infection.
- FAM26F downregulation is a characteristic feature of HBV infection.
- FAM26F expression warrants further investigation as a potential early predictive biomarker for HBV infection.
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