MHV68 Latency Modulates the Host Immune Response to Influenza A Virus |
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Authors: | Fumitake Saito Toshihiro Ito Judith M. Connett Matthew A. Schaller William F. Carson IV Cory M. Hogaboam Rosemary Rochford Steven L. Kunkel |
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Affiliation: | 1. Division of Pulmonary Medicine, Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160-8582, Japan 2. Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan 3. Immunology Program, Department of Pathology, University of Michigan Medical School 4701 BSRB, 109 Zina Pitcher Place, Ann Arbor, MI, 48109-2200, USA 4. Department of Immunol/Micro, SUNY Upstate Med Univ, Syracuse, NY, USA
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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. |
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