An Antiviral Role for TRIM14 in Ebola Virus Infection

TRIM14 在埃博拉病毒感染中的抗病毒作用

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作者:Makoto Kuroda, Peter J Halfmann, Larissa B Thackray, Michael S Diamond, Heinz Feldmann, Andrea Marzi, Yoshihiro Kawaoka0

Abstract

Ebola virus (EBOV) is a highly pathogenic virus that encodes 7 multifunctional structural proteins. Multiple host factors have been reported to interact with the EBOV proteins. Here, we found that tripartite motif-containing 14 (TRIM14), an interferon-stimulated gene that mediates cellular signaling pathways associated with type I interferon and inflammatory cytokine production, interacts with EBOV nucleoprotein to enhance interferon-β (IFN-β) and nuclear factor-κB (NF-κB) promotor activation. Moreover, TRIM14 overexpression reduced viral replication in an infectious but biologically contained EBOVΔVP30 system by approximately 10-fold without affecting viral protein expression. Furthermore, TRM14-deficient mice were more susceptible to mouse-adapted EBOV infection than wild-type mice. Our data suggest that TRIM14 is a host factor with anti-EBOV activity that limits EBOV pathogenesis.

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