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STING induces early IFN-β in the liver and constrains myeloid cell-mediated dissemination of murine cytomegalovirus

Author

Listed:
  • Pia-Katharina Tegtmeyer

    (Institute for Experimental Infection Research)

  • Julia Spanier

    (Institute for Experimental Infection Research)

  • Katharina Borst

    (Institute for Experimental Infection Research
    University of Freiburg)

  • Jennifer Becker

    (Institute for Experimental Infection Research)

  • André Riedl

    (University of Freiburg)

  • Christoph Hirche

    (Institute for Experimental Infection Research)

  • Luca Ghita

    (Institute for Experimental Infection Research)

  • Jennifer Skerra

    (Institute for Experimental Infection Research)

  • Kira Baumann

    (Institute for Experimental Infection Research)

  • Stefan Lienenklaus

    (Institute for Experimental Infection Research
    Hanover Medical School)

  • Marius Doering

    (Institute for Experimental Infection Research
    PSL Research University, INSERM U932)

  • Zsolt Ruzsics

    (University of Freiburg)

  • Ulrich Kalinke

    (Institute for Experimental Infection Research
    Hanover Medical School)

Abstract

Cytomegalovirus is a DNA-encoded β-herpesvirus that induces STING-dependent type 1 interferon responses in macrophages and uses myeloid cells as a vehicle for dissemination. Here we report that STING knockout mice are as resistant to murine cytomegalovirus (MCMV) infection as wild-type controls, whereas mice with a combined Toll-like receptor/RIG-I-like receptor/STING signaling deficiency do not mount type 1 interferon responses and succumb to the infection. Although STING alone is dispensable for survival, early IFN-β induction in Kupffer cells is STING-dependent and controls early hepatic virus propagation. Infection experiments with an inducible reporter MCMV show that STING constrains MCMV replication in myeloid cells and limits viral dissemination via these cells. By contrast, restriction of viral dissemination from hepatocytes to other organs is independent of STING. Thus, during MCMV infection STING is involved in early IFN-β induction in Kupffer cells and the restriction of viral dissemination via myeloid cells, whereas it is dispensable for survival.

Suggested Citation

  • Pia-Katharina Tegtmeyer & Julia Spanier & Katharina Borst & Jennifer Becker & André Riedl & Christoph Hirche & Luca Ghita & Jennifer Skerra & Kira Baumann & Stefan Lienenklaus & Marius Doering & Zsolt, 2019. "STING induces early IFN-β in the liver and constrains myeloid cell-mediated dissemination of murine cytomegalovirus," Nature Communications, Nature, vol. 10(1), pages 1-12, December.
  • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-10863-0
    DOI: 10.1038/s41467-019-10863-0
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    Cited by:

    1. Katarzyna M. Sitnik & Fran Krstanović & Natascha Gödecke & Ulfert Rand & Tobias Kubsch & Henrike Maaß & Yeonsu Kim & Ilija Brizić & Luka Čičin-Šain, 2023. "Fibroblasts are a site of murine cytomegalovirus lytic replication and Stat1-dependent latent persistence in vivo," Nature Communications, Nature, vol. 14(1), pages 1-13, December.

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