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Infection

The interferon paradox

Nature Reviews Immunology volume 13, pages 392–393 (2013)Cite this article

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In both studies, mice were infected with one of two strains of lymphocytic choriomeningitis virus (LCMV): the Armstrong LCMV strain, which induces robust virus-specific CD8+ T cell responses, was used to model acute viral infection; and the C113 LCMV strain, which persists systemically for more than 70 days post-infection, was used to mimic chronic viral infection. Wilson et al. observed long-term expression of type I IFN and ISGs in mice with chronic LCMV infection but not in those with acute LCMV infection. Moreover, Teijaro et al. found that C113 LCMV (but not Armstrong LCMV) targeted plasmacytoid dendritic cells (DCs) to induce the expression of type I IFN very early after infection. So, the type I IFN response seems to be elevated during chronic infection, and both groups associated this with the increased expression of immunosuppressive genes, such as interleukin-10 (Il10) and programmed cell death 1 ligand 1 (Pdl1), in C113 LCMV-infected mice.

the therapeutic potential of inhibitors of type I IFN signalling should now be investigated in patients with chronic viral infections

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References

  1. Wilson, E. B. et al. Blockade of chronic type I interferon signalling to control persistent LCMV infection. Science 340, 202–207 (2013)

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  2. Teijaro, J. R. et al. Persistent LCMV infection is controlled by blockade of type I interferon signalling. Science 340, 207–211 (2013)

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Authors
  1. Maria Papatriantafyllou
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Papatriantafyllou, M. The interferon paradox. Nat Rev Immunol 13, 392–393 (2013). https://doi.org/10.1038/nri3461

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