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miR-124 attenuates Japanese encephalitis virus replication by targeting DNM2
Songbai Yang1, Yue Pei1, Xinyun Li2
1College of Animal Science and Technology, Zhejiang A&F University, Lin'an, Zhejiang, 311300, China.
Background:
Japanese encephalitis virus (JEV) is a mosquito-borne flavivirus that causes acute viral encephalitis in humans. Pigs are important amplifier hosts of JEV. Emerging evidence indicates that host microRNAs (miRNAs) play key roles in modulating viral infection and pathogenesis. However, mechanistic studies delineating the roles of miRNAs in regulating host-JEV interactions remain scarce.
Results:
In this study, we demonstrated that miR-124 inhibited JEV replication in porcine kidney epithelial PK15 cells. Furthermore, using bioinformatics tools, we identified dynamin2 (DNM2), a GTPase responsible for vesicle scission, as a target of miR-124. Small interfering RNA (siRNA) depletion studies inicated that dynamin2 was required for efficient JEV replication. We also demonstrated that upregulation of miR-124 expression corresponded to decreased expression of its target, DNM2, in the JEV-infected PK15 cells.
Conclusions:
Overall, these results suggest the importance of miR-124 in modulating JEV replication and provide a scientific basis for using cellular miRNAs in anti-JEV therapies.
Insights
MicroRNA-124 (miR-124) inhibits Japanese encephalitis virus (JEV) replication in pigs. This study identifies dynamin2 as a target of miR-124, offering potential for new anti-JEV therapies.
Area of Science:
- Virology
- Molecular Biology
- Immunology
Background:
- Japanese encephalitis virus (JEV) causes acute viral encephalitis.
- Pigs serve as critical amplifier hosts for JEV.
- Host microRNAs (miRNAs) are increasingly recognized for their role in viral infections, yet their specific functions in JEV pathogenesis are not fully understood.
Purpose of the Study:
- To investigate the role of specific host miRNAs in regulating JEV replication.
- To identify the molecular targets of miRNAs involved in JEV-host interactions.
- To explore the potential of miRNAs as therapeutic agents against JEV.
Main Methods:
- Utilized porcine kidney epithelial PK15 cells for JEV infection studies.
- Employed bioinformatics to predict miRNA targets.
- Conducted small interfering RNA (siRNA) depletion experiments to validate target function.
- Quantified miRNA and target gene expression levels.
Main Results:
- Demonstrated that miR-124 significantly inhibits JEV replication in PK15 cells.
- Identified dynamin2 (DNM2), a key protein in vesicle formation, as a direct target of miR-124.
- Confirmed that DNM2 is essential for efficient JEV replication.
- Observed a negative correlation between miR-124 upregulation and DNM2 expression in JEV-infected cells.
Conclusions:
- miR-124 plays a crucial role in controlling JEV replication.
- The miR-124/DNM2 interaction provides a novel mechanism in host-JEV interplay.
- These findings support the development of miRNA-based strategies for anti-JEV therapies.
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