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MiR-155-5p modulates HSV-1 replication via the epigenetic regulation of SRSF2 gene expression
A previous study reported that miR-155-5p knockout mice were more resistant to herpes simplex virus type I (HSV-1) infection. However, the exact underlying molecular mechanism remains to be elucidated. Here, we demonstrated that HSV-1 infection upregulates miR-155-5p expression. By binding to the pr...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Taylor & Francis
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6557561/ https://www.ncbi.nlm.nih.gov/pubmed/30950329 http://dx.doi.org/10.1080/15592294.2019.1600388 |
Sumario: | A previous study reported that miR-155-5p knockout mice were more resistant to herpes simplex virus type I (HSV-1) infection. However, the exact underlying molecular mechanism remains to be elucidated. Here, we demonstrated that HSV-1 infection upregulates miR-155-5p expression. By binding to the promoter of serine/arginine-rich splicing factor 2 (SRSF2), which is an important transcriptional activator of HSV-1 genes that was previously reported by our group, and altering the histone modification located near the transcription start site (TSS) of the SRSF2 gene, miR-155-5p promotes the transcription of the SRSF2 gene, ultimately increasing viral replication and viral gene expression. Our results provide insight for an understanding of the roles and molecular mechanism of miR-155-5p in HSV-1 replication and the epigenetic control of SRSF2 gene expression. |
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