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Herpesvirus latency confers symbiotic protection from bacterial infection

Author

Listed:
  • Erik S. Barton

    (Departments of Pathology and Immunology,
    Present address: Purdue University, Department of Biological Sciences, 915 W. State Street, West Lafayette, Indiana 47907, USA.)

  • Douglas W. White

    (Departments of Pathology and Immunology,
    Washington University Medical School, 660 South Euclid Avenue, St. Louis, Missouri 63110, USA)

  • 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,
    Molecular Microbiology,
    Medicine, and,)

  • Virginia L. Miller

    (Molecular Microbiology,
    Pediatrics, and,)

  • Herbert W. Virgin

    (Departments of Pathology and Immunology,
    Molecular Microbiology,)

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.

Suggested Citation

  • Erik S. Barton & Douglas W. White & Jason S. Cathelyn & Kelly A. Brett-McClellan & Michael Engle & Michael S. Diamond & Virginia L. Miller & Herbert W. Virgin, 2007. "Herpesvirus latency confers symbiotic protection from bacterial infection," Nature, Nature, vol. 447(7142), pages 326-329, May.
    • Handle: RePEc:nat:nature:v:447:y:2007:i:7142:d:10.1038_nature05762
    DOI: 10.1038/nature05762
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    Cited by:

    1. Yan Jiang & Siqi Sun & Yuan Quan & Xin Wang & Yuling You & Xiao Zhang & Yue Zhang & Yin Liu & Bingjing Wang & Henan Xu & Xuetao Cao, 2023. "Nuclear RPSA senses viral nucleic acids to promote the innate inflammatory response," Nature Communications, Nature, vol. 14(1), pages 1-14, December.
    2. Philipp Walch & Petr Broz, 2024. "Viral-bacterial co-infections screen in vitro reveals molecular processes affecting pathogen proliferation and host cell viability," Nature Communications, Nature, vol. 15(1), pages 1-16, December.
    3. José Camacho Mateu & Matteo Sireci & Miguel A Muñoz, 2021. "Phenotypic-dependent variability and the emergence of tolerance in bacterial populations," PLOS Computational Biology, Public Library of Science, vol. 17(9), pages 1-28, September.

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