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Updated: May 10, 2026
Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus
Published on: October 7, 2011
MHV68 latency modulates the host immune response to influenza A virus
Fumitake Saito1, Toshihiro Ito, Judith M Connett
1Division of Pulmonary Medicine, Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160-8582, Japan.
Abstract:
Murine gammaherpesvirus 68 (MHV68) is a natural rodent pathogen that has been used as a model to study the pathogenesis of human gammaherpesviruses. Like other herpesviruses, MHV68 causes acute infection and establishes life-long latency in the host. Recently, it has been shown that mice latently infected with MHV68 have resistance to unrelated pathogens in secondary infection models. We therefore hypothesized that latent MHV68 infection could modulate the host response to influenza A virus. To test this hypothesis, mice were infected intranasally with influenza virus following the establishment of MHV68 latency. Mice latently infected with MHV68 showed significantly higher survival to influenza A virus infection than did PBS mock-infected mice. Latent MHV68 infection led to lower influenza viral loads and decreased inflammatory pathology in the lungs. Alveolar macrophages of mice latently infected with MHV68 showed activated status, and adoptive transfer of those activated macrophages into mice followed the infection with influenza A virus had significantly greater survival rates than control mice, suggesting that activated alveolar macrophages are a key mechanistic component in protection from secondary infections.
Insights
Latent murine gammaherpesvirus 68 infection enhances survival against influenza A virus. This protection is mediated by activated alveolar macrophages, reducing viral load and lung inflammation.
Area of Science:
- Virology
- Immunology
- Pathogenesis
Background:
- Murine gammaherpesvirus 68 (MHV68) is a model for human gammaherpesviruses, establishing lifelong latency.
- Latent MHV68 infection has been linked to resistance against unrelated pathogens in secondary infections.
Purpose of the Study:
- To investigate if latent MHV68 infection modulates the host immune response to influenza A virus.
- To determine the role of alveolar macrophages in MHV68-mediated protection against secondary infections.
Main Methods:
- Mice with established latent MHV68 infection were challenged with influenza A virus.
- Influenza viral loads, lung pathology, and alveolar macrophage activation status were assessed.
- Adoptive transfer of activated alveolar macrophages was performed to evaluate their protective role.
Main Results:
- Mice with latent MHV68 infection exhibited significantly higher survival rates following influenza A virus challenge compared to controls.
- Latent MHV68 infection resulted in reduced influenza viral loads and decreased lung inflammatory pathology.
- Activated alveolar macrophages from latently infected mice conferred enhanced survival in recipient mice challenged with influenza A virus.
Conclusions:
- Latent MHV68 infection confers significant protection against secondary influenza A virus infection.
- Activated alveolar macrophages are a key mechanism underlying this protective effect.
- MHV68 latency can reprogram macrophage function, offering resistance to unrelated viral pathogens.
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