Herpesvirus latency confers symbiotic protection from bacterial infection

Erik S. Barton, Douglas W. White, Jason S. Cathelyn, Kelly A. Brett-McClellan, Michael Engle, Michael S. Diamond, Virginia L. Miller and Herbert W. Virgin ()
Additional contact information
Erik S. Barton: Departments of Pathology and Immunology,
Douglas W. White: Departments of Pathology and Immunology,
Jason S. Cathelyn: Molecular Microbiology,
Kelly A. Brett-McClellan: Departments of Pathology and Immunology,
Michael Engle: Medicine, and,
Michael S. Diamond: Departments of Pathology and Immunology,
Virginia L. Miller: Molecular Microbiology,
Herbert W. Virgin: Departments of Pathology and Immunology,

Nature, 2007, vol. 447, issue 7142, 326-329

Abstract: A new angle on herpes The conventional view of herpesvirus infections is that they are either active and harmful, or at best silent and for the time being harmless. But new work on mice suggests a third option: there may be a direct benefit for chronic herpesvirus infection. Latent infection with the murine γHV68 confers prolonged cross-protection against a variety of bacterial pathogens, including Listeria and the plague bacillus. The protection is a result of systemic macrophage activation triggered by γ-interferon. The latent virus thereby sets the level of innate immunity. Not only is latency an active immunologic state, but this activity provides symbiotic benefit.

Date: 2007
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DOI: 10.1038/nature05762

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