USP18 Mediates Interferon Resistance of Dengue Virus Infection
Interferon-stimulated gene
STAT1
STAT2
ISG15
HeLa
DOI:
10.3389/fmicb.2021.682380
Publication Date:
2021-04-30T04:57:50Z
AUTHORS (8)
ABSTRACT
Previous studies demonstrated that dengue virus (DENV) infection developed resistance to type-I interferons (IFNα/β). The underlying mechanism remains unclear. USP18 is a negative regulator of IFNα/β signaling, and its expression level significantly increased following DENV in cell lines patients’ blood. Our previous study revealed contributed the IFN-α Hepatitis C Virus (HCV). However, role replication elusive. In this current study, we aimed explore DENV-2 IFN-α. was up-regulated by plasmid transfection down-regulated siRNA Hela cells. USP18, IFN-α, IFN-β expression, were monitored qRT-PCR Western blot. activation Jak/STAT signaling pathway assessed at three levels: p-STAT1/p-STAT2 (Western blot), interferon-stimulated response element (ISRE) activity (Dual-luciferase assay), genes (ISGs) (qRT-PCR). data showed overexpression promoted replication, while silence inhibited replication. Silence potentiated anti-DENV-2 through IFN-α-mediated as shown p-STAT1/p-STAT2, enhanced ISRE activity, elevated some ISGs. indicated induced critical host factor utilized confer antagonism on
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