PARP12 suppresses Zika virus infection through PARP-dependent degradation of NS1 and NS3 viral proteins
Zika virus infection stimulates a type I interferon (IFN) response in host cells, which suppresses viral replication. Type I IFNs exert antiviral effects by inducing the expression of hundreds of IFN-stimulated genes (ISGs). To screen for antiviral ISGs that restricted Zika virus replication, we individually knocked out 21 ISGs in A549 lung cancer cells and identified PARP12 as a strong inhibitor of Zika virus replication. Our findings suggest that PARP12 mediated the ADP-ribosylation of NS1 and NS3, nonstructural viral proteins that are involved in viral replication and modulating host defense responses. This modification of NS1 and NS3 triggered their proteasome-mediated degradation. These data increase our understanding of the antiviral activity of PARP12 and suggest a molecular basis for the potential development of therapeutics against Zika virus.
Source: Signal Transduction Knowledge Environment - Category: Science Authors: Li, L., Zhao, H., Liu, P., Li, C., Quanquin, N., Ji, X., Sun, N., Du, P., Qin, C.-F., Lu, N., Cheng, G. Tags: STKE Research Articles Source Type: news
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