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Updated: Aug 11, 2026
Influenza A Virus Studies in a Mouse Model of Infection
Published on: September 7, 2017
Activity of cyclosporin A in experimental influenza virus infection in mice
Abstract:
Oral administration of the immunosuppressive fungal metabolite cyclosporin A increased the mortality of Balb/c mice infected intranasally with influenza A/Hong Kong/1/68 (H3N2) virus. Cyclosporin A also increased the amount of virus that could be recovered from the lungs of infected mice and delayed the rate at which it was eliminated. Treatment with cyclosporin A did not, however, prevent the appearance of haemagglutination inhibiting antibody in the sera of animals that had been infected with a sub-lethal concentration of virus.
Insights
Oral cyclosporin A (immunosuppressive drug) worsened outcomes in mice infected with influenza A virus. It increased mortality, viral load in lungs, and delayed virus clearance, despite not affecting antibody response.
Area of Science:
- Immunology
- Virology
- Pharmacology
Background:
- Influenza A virus poses a significant public health threat.
- Immunosuppressive agents can alter host-pathogen interactions.
- Cyclosporin A is a potent immunosuppressive metabolite.
Purpose of the Study:
- To investigate the effect of cyclosporin A on influenza A virus infection in a mouse model.
- To determine if cyclosporin A impacts viral load, clearance, and host mortality.
Main Methods:
- Balb/c mice were infected intranasally with influenza A/Hong Kong/1/68 (H3N2) virus.
- Mice received oral administration of cyclosporin A.
- Viral load in lungs, mortality, and antibody response were assessed.
Main Results:
- Cyclosporin A significantly increased mortality in infected mice.
- Increased viral recovery from lungs was observed in cyclosporin A treated mice.
- Delayed viral clearance and unaffected hemagglutination inhibition antibody response were noted.
Conclusions:
- Oral cyclosporin A exacerbates influenza A virus infection in mice.
- Immunosuppression by cyclosporin A impairs the host's ability to control viral infection.
- Further research is needed to understand the mechanisms underlying this interaction.
