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IFNα and β Mediated JCPyV Suppression through C/EBPβ-LIP Isoform
Dana May1, Anna Bellizzi1, Workineh Kassa2
1Department of Neuroscience, Center for Neurovirology-Lewis Katz School of Medicine at Temple University, 3500 N. Broad Street, Philadelphia, PA 19140, USA.
Viruses
|October 26, 2021
Summary
Interferon-alpha (IFNα) and interferon-beta (IFNβ) suppress JC polyomavirus (JCPyV) replication by increasing liver inhibitory protein (LIP), an isoform of C/EBPβ. This mechanism may control JCPyV latency and reactivation in PML.
Area of Science:
- Virology
- Immunology
- Neuroscience
Background:
- JC polyomavirus (JCPyV) causes progressive multifocal leukoencephalopathy (PML), a severe demyelinating disease.
- JCPyV reactivation under immunosuppression is linked to glial cell infection and viral gene expression.
- Tumor necrosis factor-alpha (TNF-α) stimulates JCPyV transcription, but regulatory mechanisms remain incompletely understood.
Purpose of the Study:
- To investigate the role of interferon-alpha (IFNα) and interferon-beta (IFNβ) in regulating JCPyV transcription and replication.
- To elucidate the mechanism by which interferons exert their regulatory effects on JCPyV.
- To determine the involvement of C/EBPβ-LIP in interferon-mediated JCPyV suppression.
Main Methods:
- Treatment of glial cell lines with IFNα or IFNβ.
- Analysis of JCPyV transcriptional regulation and viral replication.
- Assessment of C/EBPβ-LIP expression levels.
- Knockdown of C/EBPβ-LIP using short hairpin RNA (shRNA).
Main Results:
- IFNα and IFNβ were found to negatively regulate JCPyV transcriptional regulation.
- Interferons induce the expression of liver inhibitory protein (LIP), an isoform of C/EBPβ, in glial cells.
- The inhibitory effect of interferons on JCPyV transcription and replication is enhanced by C/EBPβ-LIP.
- Knockdown of C/EBPβ-LIP reversed the inhibitory effects of interferons on JCPyV replication.
Conclusions:
- IFNα and IFNβ negatively regulate JCPyV through the induction of C/EBPβ-LIP.
- C/EBPβ-LIP plays a critical role in mediating the antiviral effects of interferons against JCPyV.
- This interferon-C/EBPβ-LIP pathway may be a key factor in controlling the balance between JCPyV latency and reactivation.
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