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TRIM27 Promotes Hepatitis C Virus Replication by Suppressing Type I Interferon Response

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Abstract

Type I interferon (IFN) response is central for host defense against viral infection. Tripartite motif 27 (TRIM27) is implicated in antiviral innate immune response; however, whether it affects the replication of hepatitis C virus (HCV) and the underlying mechanisms remain uncharacterized. Here, we show that TRIM27 expression is induced in Huh7.5 human hepatoma cells infected with HCV or stimulated with type I IFNs in vitro. In addition, TRIM27 overexpression increases and its knockdown decreases viral RNA and protein levels, suggesting that TRIM27 positively regulates HCV replication. Mechanistically, TRIM27 inhibits type I IFN response against HCV infection through inhibiting IRF3 and NF-κB pathways, since TRIM27 mutant unable to inhibit these two inflammatory pathways fails to promote HCV replication. Taken together, this study identifies TRIM27 as a novel positive regulator of HCV replication, and also implicates that targeting TRIM27 may serve as a therapeutic strategy for controlling HCV replication.

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Correspondence to Feng Zheng.

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All experimental protocols were approved by the Ethics Committee of Qilu Hospital of Shandong University.

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Zheng, F., Xu, N. & Zhang, Y. TRIM27 Promotes Hepatitis C Virus Replication by Suppressing Type I Interferon Response. Inflammation 42, 1317–1325 (2019). https://doi.org/10.1007/s10753-019-00992-5

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