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Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
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Published on: March 2, 2014

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Blockade of interferon Beta, but not interferon alpha, signaling controls persistent viral infection

Cherie T Ng1, Brian M Sullivan1, John R Teijaro1

  • 1Department of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA 92037, USA.

Cell Host & Microbe
|May 15, 2015
PubMed

Insights

Type I interferons (IFN-I) can promote persistent viral infections. Blocking interferon-beta (IFNβ) accelerated virus clearance by improving T cell responses, while blocking interferon-alpha (IFNα) worsened viral spread.

Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • Type I interferons (IFN-I) are crucial for antiviral immunity but can also drive pathogenesis in persistent viral infections.
  • High IFN-I signatures characterize persistent infections, suggesting a dual role in disease progression.
  • Lymphocytic choriomeningitis virus (LCMV) infection models exhibit elevated IFN-I early on, and blocking the IFN-I receptor (IFNAR) enhances viral clearance.

Purpose of the Study:

  • To elucidate the distinct roles of interferon-beta (IFNβ) and interferon-alpha (IFNα) in controlling persistent LCMV infection.
  • To investigate how individual IFN-I subtypes influence viral dissemination, lymphoid structure, lymphocyte migration, and T cell responses.
  • To determine which IFN-I subtype is primarily responsible for promoting viral persistence.

Main Methods:

  • Utilized a lymphocytic choriomeningitis virus (LCMV) infection model in mice.
  • Employed targeted blockade of IFNβ or IFNα signaling pathways.
  • Assessed viral load, viral dissemination, lymphoid tissue architecture, lymphocyte migration patterns, and T cell-mediated antiviral responses.

Main Results:

  • Blocking IFNβ alone did not affect early viral spread but was critical for maintaining lymphoid structure, facilitating lymphocyte migration, and promoting robust anti-viral T cell responses, leading to accelerated viral clearance.
  • Blocking IFNα did not improve viral control and was associated with increased early viral dissemination.
  • IFNβ blockade mimicked the effects of general IFNAR blockade in terms of viral clearance, highlighting its significant role in controlling LCMV.

Conclusions:

  • Interferon-beta (IFNβ) and interferon-alpha (IFNα), despite sharing the same receptor (IFNAR), possess distinct and separable biological functions in viral infections.
  • IFNβ plays a critical role in orchestrating adaptive immune responses necessary for viral clearance during persistent LCMV infection.
  • IFNβ is identified as the primary interferon subtype responsible for promoting viral persistence in this model.

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