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Updated: Aug 19, 2026

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
Viruses evade the immune system through type I interferon-mediated STAT2-dependent, but STAT1-independent, signaling
Bumsuk Hahm1, Matthew J Trifilo, Elina I Zuniga
1Division of Virology, Department of Neuropharmacology, Department of Infectology , The Scripps Research Institute, La Jolla, California 92037, USA.
Abstract:
Understanding, treating, and preventing diseases caused by immunosuppression and/or persistent infections remain both a major challenge in biomedical research and an important health goal. For a virus or any infectious agent to persist, it must utilize strategies to suppress or evade the host's immune response. Here, we report that two dissimilar viruses employ a common maneuver to cause a profound immunosuppression. Measles virus (MV) and lymphocytic choriomeningitis virus (LCMV) interfere with dendritic cell (DC) development and expansion in vivo and in vitro. The underlying mechanism for this is through the generation of type I interferon (IFN) that acts via a signal transducer and activator of a transcription (STAT)2-dependent, but STAT1-independent, pathway. Thus, viruses subvert the known antiviral effect of type I IFN through STAT2-specific signaling to benefit their survival. These observations have implications for understanding and developing therapies to treat diseases caused by immunosuppression and/or persistent infections.
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