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Targeting the pro-inflammatory factor CCL2 (MCP-1) with Bindarit for influenza A (H7N9) treatment
Stefan Wolf1,2, Scott Johnson1, Olivia Perwitasari1
1Department of Infectious Diseases, University of Georgia, Athens, GA, USA.
Abstract:
Influenza A viruses are important human and animal pathogens. Seasonal influenza viruses cause infections every year, and occasionally zoonotic viruses emerge to cause pandemics with significantly higher morbidity and mortality rates. Three cases of laboratory confirmed human infection with avian influenza A (H7N9) virus were reported in 2013, and there have been several cases reported across South East Asia, and recently in North America. Most patients experience severe respiratory illness, with mortality rates approaching 40%. No vaccine is currently available and the use of antivirals is complicated due to the emergence of drug resistant strains. Thus, there is a need to identify new drugs for therapeutic intervention and disease control. In humans, following H7N9 infection, there is excessive expression of pro-inflammatory factors CCL2, IL-6, IL-8, IFNα, interferon-γ, IP-10, MIG and macrophage inflammatory protein-1β, which has been shown to contribute to fatal disease outcomes in mouse models of infection. In the current study, the potent inhibitor of CCL2 synthesis, Bindarit, was examined as a countermeasure for H7N9-induced inflammation in a mouse model. Bindarit treatment of mice did not have any substantial therapeutic efficacy in H7N9 infection. Consequently, the results suggest that Bindarit may be ill-advised in the treatment of influenza H7N9 infection.
Insights
Bindarit, an inhibitor of CCL2 synthesis, was tested against avian influenza A (H7N9) virus infection. The study found Bindarit did not effectively treat H7N9-induced inflammation or improve outcomes in a mouse model.
Area of Science:
- Virology
- Immunology
- Pharmacology
Background:
- Avian influenza A (H7N9) virus poses a significant threat, causing severe respiratory illness and high mortality rates in humans.
- Emerging zoonotic influenza strains like H7N9 present pandemic potential, with limited therapeutic options due to lack of vaccines and antiviral resistance.
- H7N9 infection triggers excessive pro-inflammatory factors, contributing to severe disease, as observed in human cases and mouse models.
Purpose of the Study:
- To evaluate the therapeutic potential of Bindarit, a CCL2 synthesis inhibitor, as a countermeasure against H7N9-induced inflammation and disease.
- To determine if targeting CCL2 with Bindarit can mitigate the severe outcomes associated with H7N9 viral infections.
Main Methods:
- A mouse model of H7N9 infection was utilized to assess the efficacy of Bindarit treatment.
- Mice were treated with Bindarit, and the impact on H7N9-induced inflammation and disease progression was monitored.
Main Results:
- Bindarit treatment did not demonstrate substantial therapeutic efficacy in mice infected with the H7N9 virus.
- The administration of Bindarit did not significantly alter the course of H7N9 infection or reduce disease severity in the experimental model.
Conclusions:
- The findings suggest that Bindarit may not be a suitable therapeutic agent for treating H7N9 influenza infections.
- Targeting CCL2 synthesis with Bindarit is unlikely to be an effective strategy for managing H7N9-induced inflammation and disease.
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