Type I interferon signaling drives the expression of hundreds of interferon-stimulated genes (ISGs) that are critical for host and cellular defense against viral infection. To identify ISGs that limit Zika virus infection, Li et al . screened CRISPR knockout cell lines and found that loss of PARP12 increased viral replication. Truncation and pharmacological inhibition of PARP12 indicated that antiviral activity required the PARP domain–dependent ADP-ribosylation of required viral proteins, which led to their ubiquitylation and degradation. This work identifies a distinct antiviral mechanism and suggests that PARP agonists may have clinical utility if repurposed as treatments for Zika virus.See it on Scoop.it, via Viruses, Immunology & Bioinformatics from Virology.uvic.ca
PARP12 suppresses Zika virus infection through PARP-dependent degradation of NS1 and NS3 viral proteins
Source: Viral Bioinformatics

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