ArticleMolecular biotechnology2013
Cross-protective effect of antisense oligonucleotide developed against the common 3' NCR of influenza A virus genome.
Article in Molecular biotechnology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- Biomedical Applications of Antiviral Nanohybrid Materials Relating to the COVID-19 Pandemic and Other Viral Crises.Polymers · 2021Review
- Coronavirus RNA Proofreading: Molecular Basis and Therapeutic Targeting.Molecular cell · 2020Review
- Emerging Influenza D Virus Threat: What We Know so Far!Journal of clinical medicine · 2019Review
- Advancements in Nucleic Acid Based Therapeutics against Respiratory Viral Infections.Journal of clinical medicine · 2018Review
- The emerging influenza virus threat: status and new prospects for its therapy and control.Archives of virology · 2018Review
- High antiviral effect of TiOBeilstein journal of nanotechnology · 2016Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The influenza A virus (IAV) has eight segmented single-stranded RNA genome containing a common and evolutionarily conserved non-coding region (NCRs) at 5' and 3' ends that are important for the virus replication. In this study, we designed an antisense oligonucleotide against the 3' NCR of vital segments of the IAV genome to inhibit its replication. The results demonstrated that the co-transfection of Madine Darby Canine Kidney (MDCK) cells with the antisense oligonucleotide and the plasmids encoding the viral genes led to the down-regulation of the viral gene expression. The designed antisense molecules reduced the cytopathic effect caused by A/PR/8/34 (H1N1), A/Udorn/307/72 (H3N2), and A/New Caledonia/20/99 (H1N1) strains of IAV for almost 48 h. Furthermore, the intra-venous delivery of this oligonucleotide significantly reduced the viral titers in the lungs of infected mice and protected the mice from lethal effects of all the strains of influenza virus. The study demonstrated that the antisense oligonucleotide designed against the NCR region inhibits the expression of the viral genome. The decrease of the cytopathic effect in the MDCK cells and increase in survival of mice confirmed the reduction of virus multiplication and pathogenesis in the presence of antisense oligonucleotide. Thus, we demonstrate that a single antisense oligonucleotide is capable of providing protection against more than one strains of the IAV.
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