ArticlePloS one2012
Cyclosporin A inhibits the influenza virus replication through cyclophilin A-dependent and -independent pathways.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.
- Dynamic data-driven meta-analysis for prioritisation of host genes implicated in COVID-19.Scientific reports · 2020Pooled it
- Effectiveness and safety of cyclosporine A in moderate to severe COVID-19: a randomized, open-label trial.Scientific reports · 2026Trial
- Article
- Article
- Influenza A virus exploits transferrin receptor recycling to enter host cells.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Review
- Repurposing of cyclophilin A inhibitors as broad-spectrum antiviral agents.Drug discovery today · 2022Review
- Emerging Roles of Cyclophilin A in Regulating Viral Cloaking.Frontiers in microbiology · 2022Review
- Target Discovery for Host-Directed Antiviral Therapies: Application of Proteomics Approaches.mSystems · 2021Article
- Human respiratory viral infections: Current status and future prospects of nanotechnology-based approaches for prophylaxis and treatment.Life sciences · 2021Review
- Development of Broad-Spectrum Antiviral Agents-Inspiration from Immunomodulatory Natural Products.Viruses · 2021Review
- Drug repurposing screens reveal cell-type-specific entry pathways and FDA-approved drugs active against SARS-Cov-2.Cell reports · 2021Article
- Cyclophilin A: a key player for etiological agent infection.Applied microbiology and biotechnology · 2021Review
- Strategy, Progress, and Challenges of Drug Repurposing for Efficient Antiviral Discovery.Frontiers in pharmacology · 2021Review
- Drug repurposing for new, efficient, broad spectrum antivirals.Virus research · 2019Review
- Review
- Advancements in Host-Based Interventions for Influenza Treatment.Frontiers in immunology · 2018Review
- Current landscape and future prospects of antiviral drugs derived from microbial products.The Journal of antibiotics · 2017Review
- FPR2: A Novel Promising Target for the Treatment of Influenza.Frontiers in microbiology · 2017Review
- Discovery of cyclosporine A and its analogs as broad-spectrum anti-influenza drugs with a high in vitro genetic barrier of drug resistance.Antiviral research · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The immunosuppressive drug cyclosporin A (CsA) has inhibitory effects on the replication of several viruses. The antiviral effects are through targeting the interaction between viral proteins and host factor cyclophilin A (CypA). CypA has been identified to interact with influenza A virus M1 protein and impair the early stage of the viral life cycle. In order to identify the effect of CsA on influenza virus replication, a CypA-depleted 293T cell line, which was named as 293T/CypA-, was constructed. The cytopathic effect (CPE) assay and the growth curve results indicated that CsA specifically suppressed the influenza A virus replication in a dose-dependent manner. CsA treatment had no effect on the viral genome replication and transcription but selectively suppressed the viral proteins expression. Further studies indicated that CsA could impair the nuclear export of viral mRNA in the absence of CypA. In addition, the antiviral activity of CsA was independent of calcineurin signaling. Finally, CsA could enhance the binding between CypA and M1. The above results suggested that CsA inhibited the replication of influenza A virus through CypA-dependent and -independent pathways.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.