scholarly journals Regulation of arginase II by interferon regulatory factor 3 and the involvement of polyamines in the antiviral response

FEBS Journal ◽  
2005 ◽  
Vol 272 (12) ◽  
pp. 3120-3131 ◽  
Author(s):  
Nathalie Grandvaux ◽  
François Gaboriau ◽  
Jennifer Harris ◽  
Benjamin R. TenOever ◽  
Rongtuan Lin ◽  
...  
Keyword(s):  
Interferon Regulatory Factor ◽  
Antiviral Response ◽  
Regulatory Factor ◽  
Interferon Regulatory Factor 3 ◽  
Arginase Ii

scholarly journals C6orf106 is a novel inhibitor of the interferon-regulatory factor 3–dependent innate antiviral response

2018 ◽  
Vol 293 (27) ◽  
pp. 10561-10573 ◽  
Author(s):  
Rebecca L. Ambrose ◽  
Yu Chih Liu ◽  
Timothy E. Adams ◽  
Andrew G. D. Bean ◽  
Cameron R. Stewart
Keyword(s):  
Interferon Regulatory Factor ◽  
Antiviral Response ◽  
Regulatory Factor ◽  
Interferon Regulatory Factor 3 ◽  
Innate Antiviral Response

Characterization of the interferon regulatory factor 3-mediated antiviral response in a cell line deficient for IFN production

2009 ◽  
Vol 46 (3) ◽  
pp. 393-399 ◽  
Author(s):  
Tracy Chew ◽  
Ryan Noyce ◽  
Susan E. Collins ◽  
Meaghan H. Hancock ◽  
Karen L. Mossman
Keyword(s):  
Cell Line ◽  
Interferon Regulatory Factor ◽  
Antiviral Response ◽  
Regulatory Factor ◽  
Interferon Regulatory Factor 3 ◽  
A Cell

scholarly journals West Nile Virus Evades Activation of Interferon Regulatory Factor 3 through RIG-I-Dependent and -Independent Pathways without Antagonizing Host Defense Signaling

2006 ◽  
Vol 80 (6) ◽  
pp. 2913-2923 ◽  
Author(s):  
Brenda L. Fredericksen ◽  
Michael Gale
Keyword(s):  
West Nile Virus ◽  
Host Response ◽  
Virus Production ◽  
Interferon Regulatory Factor ◽  
Antiviral Response ◽  
Productive Infection ◽  
Null Mouse ◽  
Regulatory Factor ◽  
West Nile ◽  
Interferon Regulatory Factor 3

ABSTRACT The ability of viruses to control and/or evade the host antiviral response is critical to the establishment of a productive infection. We have previously shown that West Nile virus NY (WNV-NY) delays activation of interferon regulatory factor 3 (IRF-3), a transcription factor critical to the initiation of the antiviral response. Here we demonstrate that the delayed activation of IRF-3 is essential for WNV-NY to achieve maximum virus production. Furthermore, WNV-NY utilizes a unique mechanism to control activation of IRF-3. In contrast to many other viruses that impose a nonspecific block to the IRF-3 pathway, WNV-NY eludes detection by the host cell at early times postinfection. To better understand this process, we assessed the role of the pathogen recognition receptor (PRR) retinoic acid-inducible gene I (RIG-I) in sensing WNV-NY infection. RIG-I null mouse embryo fibroblasts (MEFs) retained the ability to respond to WNV-NY infection; however, the onset of the host response was delayed compared to wild-type (WT) MEFs. This suggests that RIG-I is involved in initially sensing WNV-NY infection, while other PRRs sustain and/or amplify the host response later in infection. The delayed initiation of the host response correlated with an increase in WNV-NY replication in RIG-I null MEFs compared to WT MEFs. Our data suggest that activation of the host response by RIG-I early in infection is important for controlling replication of WNV-NY. Furthermore, pathogenic strains of WNV may have evolved to circumvent stimulation of the host response until after replication is well under way.

scholarly journals Ipr1 Regulation by Cyclic GMP-AMP Synthase/Interferon Regulatory Factor 3 and Modulation of Irgm1 Expression via p53

2020 ◽  
Vol 40 (8) ◽  
Author(s):  
Fayang Liu ◽  
Hongni Xue ◽  
Jie Ke ◽  
Yongyan Wu ◽  
Kezhen Yao ◽  
...  
Keyword(s):  
Cyclic Gmp ◽  
Viral Infections ◽  
Pathogen Resistance ◽  
Interferon Regulatory Factor ◽  
Intracellular Pathogen ◽  
Regulatory Factor ◽  
Interferon Regulatory Factor 3 ◽  
Promoter Characterization ◽  
Ribosomal Protein L11 ◽  
Pathogenic Infection

ABSTRACT Intracellular pathogen resistance 1 (Ipr1) has been found to be a mediator to integrate cyclic GMP-AMP synthase (cGAS)–interferon regulatory factor 3 (IRF3), activated by intracellular pathogens, with the p53 pathway. Previous studies have shown the process of Ipr1 induction by various immune reactions, including intracellular bacterial and viral infections. The present study demonstrated that Ipr1 is regulated by the cGAS-IRF3 pathway during pathogenic infection. IRF3 was found to regulate Ipr1 expression by directly binding the interferon-stimulated response element motif of the Ipr1 promoter. Knockdown of Ipr1 decreased the expression of immunity-related GTPase family M member 1 (Irgm1), which plays critical roles in autophagy initiation. Irgm1 promoter characterization revealed a p53 motif in front of the transcription start site. P53 was found to participate in regulation of Irgm1 expression and IPR1-related effects on P53 stability by affecting interactions between ribosomal protein L11 (RPL11) and transformed mouse 3T3 cell double minute 2 (MDM2). Our results indicate that Ipr1 integrates cGAS-IRF3 with p53-modulated Irgm1 expression.

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