A study on the relationship between HCV NS3 and endogenous IRF-3

Abstract

This study aims to investigate the relationship between hepatitis C virus (HCV) NS3/4A and endogenous interferon regulatory factor-3 (IRF-3). The localization of endogenous IRF-3 protein before and after virus infection was analyzed by immunofluorescence assay (IFA). IFA results revealed that the synergistic action of transfection and HCV virus infection could more effectively reduce the nuclear translocation of endogenous IRF-3 in HeLa cells, compared to the activation of Sendai virus infection alone. The highest nuclear translocation of endogenous IRF-3 in transfected HeLa cells occurred at 24 h after Sendai virus infection. Our study was consistent with a published paper, which revealed that HCV NS3/4A protease could suppress the activation of IRF-3 and was indispensable in the transcription of interferon (IFN)-α/β.

Regulation of cGAS‐Mediated Immune Responses and Immunotherapy

“…Several viral proteins inhibit phosphorylation of IRF, such as HCV NS3,95 KSHV ORF45,96 EBV BGLF4,3 vIRF,97 K8,98 and ubiquitin carboxyl‐terminal hydrolase L1 (UCHL1) 99. Besides, IRFs are also suppressed by KSHV vIRFs, EBV LF2, KSHV ORF50, and the cellular protein suppressor of cytokine signaling (SOCS) 1 prompted by HTLV‐1 Tax 94a.…”

“…[94b] The proteins include EBV deubiquitinase, Ectromelia virus (ECTV) encoded hostresponse modifiers (HRMs), and human T-cell leukemia virus type 1 (HTLV1) HBZ. [3] Several viral proteins inhibit phosphorylation of IRF, such as HCV NS3, [95] KSHV ORF45, [96] EBV BGLF4, [3] vIRF, [97] K8, [98] and ubiquitin carboxyl-terminal hydrolase L1 (UCHL1). [99] Besides, IRFs are also suppressed by KSHV vIRFs, EBV LF2, KSHV ORF50, and the cellular protein suppressor of cytokine signaling (SOCS) 1 prompted by HTLV-1 Tax.…”