AI Article Synopsis
- Successful replication of the influenza A virus relies on both viral proteins and host cellular factors, prompting a search for small molecules that can disrupt these components.
- The researchers utilized a reporter assay to screen a chemical compound library, leading to the discovery of compound 7, which inhibits a new target related to viral replication.
- Compound 7 demonstrated dose-dependent efficacy in reducing viral replication in lab studies and proved effective in overcoming high-dose influenza infection in a mouse model, suggesting potential for developing new anti-influenza treatments amid rising oseltamivir resistance.
Article Abstract
Successful replication of the influenza A virus requires both viral proteins and host cellular factors. In this study we used a cellular assay to screen for small molecules capable of interfering with any of such necessary viral or cellular components. We used an established reporter assay to assess influenza viral replication by monitoring the activity of co-expressed luciferase. We screened a diverse chemical compound library, resulting in the identification of compound 7, which inhibits a novel yet elusive target. Quantitative real-time PCR studies confirmed the dose-dependent inhibitory activity of compound 7 in a viral replication assay. Furthermore, we showed that compound 7 is effective in rescuing high-dose influenza infection in an in vivo mouse model. As oseltamivir-resistant influenza strains emerge, compound 7 could be further investigated as a new and potentially suitable scaffold for the development of anti-influenza agents that act on novel targets.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3769975 | PMC |
| http://dx.doi.org/10.1002/cmdc.201200453 | DOI Listing |
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