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Related Concept Videos

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The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
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Related Experiment Video

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Type I Interferon Signaling Controls Gammaherpesvirus Latency In Vivo.

Johannes Schwerk1, Lucas Kemper1, Kendra A Bussey2,3

  • 1Model System for Infection and Immunity, Helmholtz Centre for Infection Research (HZI), 38124 Braunschweig, Germany.

Pathogens (Basel, Switzerland)
|December 23, 2022
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Summary

Type I interferons (IFNs) control gammaherpesvirus latency by limiting viral spread and reactivation. Localized IFN responses are crucial for managing the reservoir of latent Epstein-Barr virus and related infections.

Keywords:
chronic infectionlatencymurine gammaherpesvirus 68type I interferon

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Area of Science:

  • Virology
  • Immunology
  • Infectious Diseases

Background:

  • Gammaherpesviruses establish lifelong latent infections, contributing to lymphoproliferative disorders and cancers.
  • Murine gammaherpesvirus 68 (MHV-68) serves as a model for studying gammaherpesvirus latency.
  • The role of type I interferon (IFN) in controlling gammaherpesvirus latency is not fully understood.

Purpose of the Study:

  • To investigate the interplay between type I IFN-mediated innate immunity and MHV-68 latency.
  • To determine if type I IFN signaling directly impacts the control of MHV-68 latency and reactivation.

Main Methods:

  • Utilized bioluminescent reporter mice to monitor type I IFN responses during MHV-68 infection.
  • Employed adoptive transfer of latently infected splenocytes into wild-type and type I IFN receptor-deficient mice.
  • Assessed viral propagation, dissemination, and reactivation in relation to type I IFN signaling.

Main Results:

  • Loss of type I IFN receptor signaling resulted in uncontrolled MHV-68 propagation and dissemination.
  • Type I IFN signaling partially controlled, but did not fully prevent, cell-to-cell transmission during latency.
  • Impaired type I IFN signaling in infected cells increased the risk of MHV-68 reactivation.

Conclusions:

  • Locally constrained type I IFN responses are critical for controlling the cellular reservoir of gammaherpesvirus latency.
  • Type I IFNs directly regulate MHV-68 latency within infected cells, preventing reactivation.
  • IFN signaling influences the distribution of latent infections to new target cells.