Key result
Overexpression of miR-101-1 in HeLa cells effectively reduced HSV-1 replication, producing less viral progeny and a weaker cytopathic effect without affecting cell viability.
Why the study?
Due to growing resistance to acyclovir, alternative treatments for HSV-1 with different mechanisms of action are required, prompting investigation into the effect of hsa-miR-101-1 on viral replication.
Does transfection of miR-101-1 reduce HSV-1 replication in HeLa cells?
Does transfection of miR-101-1 reduce HSV-1 replication in HeLa cells?
Overexpression of miR-101-1 effectively reduces HSV-1 replication in HeLa cells, suggesting a potential alternative therapeutic target for HSV-1 infections.
Could inform HSV-1 antiviral strategies; leaves open clinical translation from cell data.
INTRODUCTION: Herpes simplex viruses (HSVs) are widely distributed in the human population. HSV type 1 (HSV-1) is responsible for a spectrum of diseases, ranging from gingivostomatitis to keratoconjunctivitis, and encephalitis. The HSVs establish latent infections in nerve cells, and recurrences are common. Their frequent reactivation in elderly and immunosuppressed patients causes serious health complications. OBJECTIVES: Due to the growing resistance to its main drug, acyclovir, alternative treatments with different mechanisms of action are required. MicroRNAs regulate host and viral gene expression posttranscriptionally. Previous studies reported that mir-101-2 expression has widely participated in the regulation of HSV-1 replication. In this study, we investigate the effect of hsa-miR-101-1 in the replication of HSV-1. METHODS: We found that transfection of miR-101-1 into HeLa cells could reduce effectively HSV-1 replication using plaque assay and real-time PCR methods. RESULTS: We showed that overexpression of miR-10-1 produced less viral progeny and manifested a weaker cytopathic effect, without affecting cell viability. DISCUSSION/CONCLUSION: This result can give us new insights into the control of HSV-1 infections.
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Ehdaei et al. (2021) studied HSV-1 infection. Transfection of miR-101-1 was evaluated on HSV-1 replication. Overexpression of miR-101-1 in HeLa cells effectively reduced HSV-1 replication, producing less viral progeny and a weaker cytopathic effect without affecting cell viability.
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