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Interferon-alpha and MxA inhibit BK polyomavirus replication by interaction with polyomavirus large T antigen
Hsin-Hsu Wu1, Yi-Jung Li2, Cheng-Hao Weng2
1Kidney Research Center, Department of Nephrology, Linkou Chang Gung Memorial Hospital, Taoyuan, Taiwan; Department of Medicine, Chang Gung University, Taoyuan, Taiwan; Graduate Institute of Clinical Medical Sciences, College of Medicine, Chang Gung University, Taiwan.
Introduction:
BK Polyomavirus (BKPyV) infection is a common complication in kidney transplant recipients and can result in poor outcomes and graft failure. Currently, there is no known effective antiviral agent. This study investigated the possible antiviral effects of Interferon alpha (IFNα) and its induced protein, MxA, against BKPyV.
Methods:
In vitro cell culture experiments were conducted using human primary renal proximal tubular epithelial cells (HRPTECs). We also did animal studies using Balb/c mice with unilateral kidney ischemic reperfusion injury.
Results:
Our results demonstrated that IFNα effectively inhibited BKPyV in vitro and murine polyomavirus in animal models. Additionally, IFNα and MxA were found to suppress BKPyV TAg and VP1 production. Silencing MxA attenuated the antiviral efficacy of IFNα. We observed that MxA interacted with BKPyV TAg, causing it to remain in the cytosol and preventing its nuclear translocation. To determine MxA's essential domain for its antiviral activities, different mutant MxA constructs were generated. The MxA mutant K83A retained its interaction with BKPyV TAg, and its antiviral effects were intact. The MxA T103A mutant, on the other hand, abolished GTPase activity, lost its protein-protein interaction with BKPyV TAg, and lost its antiviral effect.
Conclusion:
IFNα and its downstream protein, MxA, have potent antiviral properties against BKPyV. Furthermore, our findings indicate that the interaction between MxA and BKVPyV TAg plays a crucial role in determining the anti-BKPyV effects of MxA.
Insights
Interferon alpha (IFNα) and its protein MxA show antiviral effects against BK Polyomavirus (BKPyV). MxA inhibits BKPyV by interacting with TAg, preventing its nuclear translocation, crucial for antiviral activity.
Area of Science:
- Virology
- Immunology
- Nephrology
Background:
- BK Polyomavirus (BKPyV) infection is a significant complication in kidney transplant recipients, leading to graft failure.
- Current treatment options for BKPyV infection are limited, with no effective antiviral agents available.
- Understanding the host immune response against BKPyV is critical for developing novel therapeutic strategies.
Purpose of the Study:
- To investigate the antiviral effects of Interferon alpha (IFNα) and its downstream protein MxA against BK Polyomavirus (BKPyV).
- To elucidate the mechanism by which MxA exerts its antiviral activity against BKPyV.
Main Methods:
- In vitro cell culture experiments using human primary renal proximal tubular epithelial cells (HRPTECs).
- In vivo animal studies involving Balb/c mice subjected to unilateral kidney ischemic reperfusion injury.
- Analysis of BKPyV TAg and VP1 production, MxA interaction with TAg, and functional assessment of MxA mutants.
Main Results:
- IFNα demonstrated effective inhibition of BKPyV in vitro and murine polyomavirus in vivo.
- Both IFNα and MxA suppressed the production of BKPyV TAg and VP1.
- MxA interaction with BKPyV TAg was essential for antiviral activity, preventing TAg nuclear translocation. MxA K83A mutant retained interaction and antiviral effect, while T103A mutant lost both.
Conclusions:
- Interferon alpha (IFNα) and its induced protein MxA possess potent antiviral properties against BKPyV.
- The interaction between MxA and BKPyV TAg is a key mechanism underlying MxA's anti-BKPyV effects.
- These findings highlight the therapeutic potential of IFNα and MxA in managing BKPyV infections, particularly in immunocompromised individuals.
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