MicroRNA‐205‐5p: A potential therapeutic target for influenza A

We are committed to finding host targets for influenza A therapeutics. The nucleoprotein (NP) plays an important role in influenza A virus replication and is an indispensable part of viral transcription and replication. Exploring endogenous substances that can modulate NP is critical for finding hos...

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Bibliographic Details
Published in:Journal of cellular and molecular medicine 2022-12, Vol.26 (23), p.5917-5928
Main Authors: Bao, Yanyan, Shi, Yujing, Zhou, Lirun, Gao, Shuangrong, Yao, Rongmei, Guo, Shanshan, Geng, Zihan, Bao, Lei, Zhao, Ronghua, Cui, Xiaolan
Format: Article
Language:English
Subjects:
Animals
Binding Sites
Chromosome 3
Complementarity
Drug dosages
Drug resistance
Gene expression
Infections
Influenza A
Influenza A virus
Laboratory animals
Lymphocytes
Lymphocytes T
Medical research
Mice
MicroRNAs
MicroRNAs - genetics
MicroRNA‐205‐5p
miRNA
NP gene
NP protein
nucleoprotein
Original
Orthomyxoviridae Infections - drug therapy
Orthomyxoviridae Infections - genetics
Oseltamivir
Physiology
Pneumonia
Replication
Reporter gene
Swine flu
therapeutic target
Therapeutic targets
Vectors
Viruses
Western blotting
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Summary:We are committed to finding host targets for influenza A therapeutics. The nucleoprotein (NP) plays an important role in influenza A virus replication and is an indispensable part of viral transcription and replication. Exploring endogenous substances that can modulate NP is critical for finding host targets. MicroRNAs (miRNAs, miR) are a novel class of powerful, endogenous gene expression regulators. Herein, we used miRanda to analyse the base complementarity between the NP gene and the 14 host miRNAs reported previously by us. MiRanda predicted that miR‐431‐5p, miR‐744‐3p and miR‐205‐5p could complement the NP gene. To understand the effect of these miRNAs on NP expression, we co‐transfected 293 T cells with NP gene sequence containing above miRNAs binding site or full sequence of NP gene (transfected into pmirGlo or pcDNA3.1 vectors, respectively), and mimics of miR‐205‐5p, miR‐431‐5p and miR‐744‐3p. Dual luciferase reporter gene or Western blotting assays confirmed that miR‐205‐5p and miR‐431‐5p inhibit NP expression by binding with the miRNA binding site of NP gene. Further, we infected Mouse Lung Epithelial (MLE‐12) cells overexpressing miR‐205‐5p and miR‐431‐5p with influenza A virus and performed Western blotting to examine NP expression. We found that NP expression was significantly reduced in MLE‐12 cells overexpressing miR‐205‐5p during influenza A infection. The miR‐205‐5p overexpression‐induced inhibition of influenza A replication could be attributed to the inhibition of NP expression. Further, we administered oseltamivir and Jinchai Antiviral Capsules (JC, an anti‐influenza Chinese medicine) to influenza A virus‐infected MLE‐12 cells and mice. We found that miR‐205‐5p was significantly decreased increased in infected cells and lung tissues, and oseltamivir and JC could up‐regulate miR‐205‐5p. In conclusion, we provide new evidence that miR‐205‐5p plays a role in regulating viral NP protein expression in combating influenza A and may be a potential target for influenza A therapy.
ISSN:1582-1838
1582-4934
DOI:10.1111/jcmm.17615