Key result
ZMPSTE24 is a host restriction factor that limits infection by a broad spectrum of enveloped viruses, acting as a downstream effector of interferon-induced transmembrane antiviral activity.
ZMPSTE24 is a key downstream effector in the interferon-induced transmembrane antiviral pathway.
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May guide antiviral drug development; leaves open clinical translation and efficacy in humans.
The zinc metalloprotease ZMPSTE24 is a constitutively and ubiquitously expressed host restriction factor that is responsible for limiting infection by a broad spectrum of enveloped viruses, including influenza A, vesicular stomatitis, zika, ebola, Sindbis, cowpox, and vaccinia viruses, but not murine leukemia or adenovirus. Antiviral function is independent of ZMPSTE24 enzymatic activity. Protein interaction and genetic complementation studies indicate that ZMPSTE24 is a component of a common antiviral pathway that is associated with interferon-induced transmembrane proteins. In vivo studies with zmpste24-deficient mice demonstrate the importance of ZMPSTE24 for antiviral defense.
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Li et al. (2017) studied Viral infection. ZMPSTE24 vs. zmpste24-deficient models was evaluated on Antiviral defense against enveloped viruses. ZMPSTE24 is a host restriction factor that limits infection by a broad spectrum of enveloped viruses, acting as a downstream effector of interferon-induced transmembrane antiviral activity.
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