Regulation of cellular innate antiviral signaling by ubiquitin modification

Lin, Dandan; Zhong, Bo

doi:10.1093/abbs/gmu133

Cited by 15 publications

(19 citation statements)

References 103 publications

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“…Recently, several reviews were published, describing the innate immune evasion strategies of individual viruses or virus families, such as influenza virus (2,3), Phleboviruses (4), Herpes viruses (5)(6)(7), Coronaviruses severe acute respiratory syndrome (SARS) and middle east respiratory syndrome (MERS) (8), human immunodeficiency virus (HIV) (9,10), as well as multiple RNA viruses (11,12). Moreover, there are recent articles that review how viruses prevent detection by pathogen recognition receptors (PRRs) (13,14) and how viruses modulate innate immune signaling by use of viral deubiquitinases (15).…”

mentioning

confidence: 99%

Viral Evasion Strategies in Type I IFN Signaling – A Summary of Recent Developments

2016

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The immune system protects the organism against infections and the damage associated with them. The first line of defense against pathogens is the innate immune response. In the case of a viral infection, it induces the interferon (IFN) signaling cascade and eventually the expression of type I IFN, which then causes an antiviral state in the cells. However, many viruses have developed strategies to counteract this mechanism and prevent the production of IFN. In order to modulate or inhibit the IFN signaling cascade in their favor, viruses have found ways to interfere at every single step of the cascade, for example, by inducing protein degradation or cleavage, or by mediate protein polyubiquitination. In this article, we will review examples of viruses that modulate the IFN response and describe the mechanisms they use.

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confidence: 99%

Viral Evasion Strategies in Type I IFN Signaling – A Summary of Recent Developments

2016

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“…Multiple TNF Receptor Associated Factors (TRAFs) have been shown to be involved in IRF-activating pathways (TRAF2, -3, -5 and -6) [ 37 ], although TRAF3 appears to more commonly play this role in most cells in vivo with TLR-dependent and -independent signaling to IRFs [ 38 , 39 , 40 , 41 ]. TRAF3 appears to play a similar role to TRAF6 in IKK complex activation by generating activating ubiquitin chains [ 42 , 43 ]. Although NEMO has been shown to play a role in TI-IFN induction, not solely for the NFκB contribution to IFNβ transactivation but also for activation of TBK1 and phosphorylation of IRF3 [ 17 , 19 ], other adapters have been suggested to play NEMO-like roles in IRF-activating complexes, such as Optineurin (OPTN) (TBK1 only) [ 44 ], TANK [ 26 ], NFκB-activating protein (NAP1) [ 45 ] and TBK1 Binding Protein 1 (TBKBP1) [ 46 ].…”

Section: Poxviral Targeting Of the Irf Family And Their Activationmentioning

confidence: 99%

Poxviral Targeting of Interferon Regulatory Factor Activation

Lawler

Brady

2020

Viruses

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As viruses have a capacity to rapidly evolve and continually alter the coding of their protein repertoires, host cells have evolved pathways to sense viruses through the one invariable feature common to all these pathogens—their nucleic acids. These genomic and transcriptional pathogen-associated molecular patterns (PAMPs) trigger the activation of germline-encoded anti-viral pattern recognition receptors (PRRs) that can distinguish viral nucleic acids from host forms by their localization and subtle differences in their chemistry. A wide range of transmembrane and cytosolic PRRs continually probe the intracellular environment for these viral PAMPs, activating pathways leading to the activation of anti-viral gene expression. The activation of Nuclear Factor Kappa B (NFκB) and Interferon (IFN) Regulatory Factor (IRF) family transcription factors are of central importance in driving pro-inflammatory and type-I interferon (TI-IFN) gene expression required to effectively restrict spread and trigger adaptive responses leading to clearance. Poxviruses evolve complex arrays of inhibitors which target these pathways at a variety of levels. This review will focus on how poxviruses target and inhibit PRR pathways leading to the activation of IRF family transcription factors.

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“…As the UPS has a vital role in many fundamental cellular processes, many viruses have reprogrammed this machinery according to their needs. The interactions between viruses and the UPS are complex; one of the more common features is the use of the UPS to control the level of antiviral factors and to regulate innate antiviral signaling (19). In the case of viruses that depend on the cell cycle, this system is used to control the level of proteins that regulate cell cycle progression, a feature observed frequently in DNA virus infections (20).…”

Section: Importancementioning

confidence: 99%

The Ubiquitin-Proteasome System Is Necessary for Efficient Replication of Human Astrovirus

Casorla-Pérez

López

2018

J Virol

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Astroviruses, members of the family , represent an important cause of human gastroenteritis in the world. The cellular factors required for astrovirus replication have been poorly studied. In this work, we evaluated the relevance of the ubiquitin-proteasome system (UPS) in the replication of Yuc8, a human astrovirus serotype 8 strain. We found that proteasome inhibitors decrease the production of infectious viral progeny at a step in the replication cycle subsequent to virus entry. The inhibition of the proteasome activity decreases viral RNA levels and viral protein synthesis; similarly, the inhibition of ubiquitination by chemical inhibitors or RNAi reduces the production of viral progeny as well as viral protein synthesis. The effect on viral progeny production induced by proteasome inhibitors is not explained by a reduction in the pool of monoubiquitin or the induction of early apoptosis or autophagy. Our observations are consistent with the need of the proteolytic activity of the UPS for the efficient replication of the virus and suggest that UPS is necessary for the production of genomic and subgenomic RNA but not for antigenomic RNA. Astroviruses are a major cause of gastroenteritis in young humans and animals and recently it has been associated to fatal encephalitis in humans. The role of ubiquitin proteasome system in the replication of these viruses has not been studied before. In this work, we present evidence that supports that the proteolytic activity of proteasome is necessary for efficient viral progeny production, and that this proteolytic system is required for the accumulation of both, the genomic and subgenomic viral RNAs.

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Regulation of cellular innate antiviral signaling by ubiquitin modification

Cited by 15 publications

References 103 publications

Viral Evasion Strategies in Type I IFN Signaling – A Summary of Recent Developments

Viral Evasion Strategies in Type I IFN Signaling – A Summary of Recent Developments

Poxviral Targeting of Interferon Regulatory Factor Activation

The Ubiquitin-Proteasome System Is Necessary for Efficient Replication of Human Astrovirus

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