To Conquer the Host, Influenza Virus Is Packing It In: Interferon-Antagonistic Strategies beyond NS1

Weber-Gerlach, Michaela; Weber, Friedemann

doi:10.1128/jvi.00041-16

Cited by 18 publications

(8 citation statements)

References 62 publications

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“…In this short review, emphasis was put on the recent identification of multiple reovirus determinants of induction and sensitivity to the antiviral interferon response. The apparent multiplicity of viral proteins involved is consistent with data obtained in the last few years with such diverse viruses as influenza, rotavirus, hepatitis C, and vesicular stomatitis virus, among others [123,124,125,126,127]. It appears that the control of the interferon response is somehow shaping the whole viral genome.…”

Section: Discussionsupporting

confidence: 85%

How Many Mammalian Reovirus Proteins are involved in the Control of the Interferon Response?

et al. 2019

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As with most viruses, mammalian reovirus can be recognized and attacked by the host-cell interferon response network. Similarly, many viruses have developed resistance mechanisms to counteract the host-cell response at different points of this response. Reflecting the complexity of the interferon signaling pathways as well as the resulting antiviral response, viruses can—and often have—evolved many determinants to interfere with this innate immune response and allow viral replication. In the last few years, it has been evidenced that mammalian reovirus encodes many different determinants that are involved in regulating the induction of the interferon response or in interfering with the action of interferon-stimulated gene products. In this brief review, we present our current understanding of the different reovirus proteins known to be involved, introduce their postulated modes of action, and raise current questions that may lead to further investigations.

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Section: Discussionsupporting

confidence: 85%

How Many Mammalian Reovirus Proteins are involved in the Control of the Interferon Response?

et al. 2019

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“…Both PB2 and PB1-F2 limit IFN production by associating with MAVS ( 10 , 34 , 35 ). Other structural proteins, such as PB1, PA, NP, and even the genomic RNA itself, also contribute to impairing RIG-I-mediated antiviral responses ( 36 ). Moreover, HA (HA1) was recently shown to drive the degradation of the IFN receptor chain IFNAR1, thereby suppressing IFN-triggered JAK/STAT signaling ( 37 ).…”

Section: Discussionmentioning

confidence: 99%

The C-Terminal Effector Domain of Non-Structural Protein 1 of Influenza A Virus Blocks IFN-β Production by Targeting TNF Receptor-Associated Factor 3

et al. 2017

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Influenza A virus non-structural protein 1 (NS1) antagonizes interferon response through diverse strategies, particularly by inhibiting the activation of interferon regulatory factor 3 (IRF3) and IFN-β transcription. However, the underlying mechanisms used by the NS1 C-terminal effector domain (ED) to inhibit the activation of IFN-β pathway are not well understood. In this study, we used influenza virus subtype of H5N1 to demonstrate that the NS1 C-terminal ED but not the N-terminal RNA-binding domain, binds TNF receptor-associated factor 3 (TRAF3). This results in an attenuation of the type I IFN signaling pathway. We found that the NS1 C-terminal ED (named NS1/126-225) inhibits the active caspase activation and recruitment domain-containing form of RIG-I [RIG-I(N)]-induced IFN-β reporter activity, the phosphorylation of IRF3, and the induction of IFN-β. Further analysis showed that NS1/126-225 binds to TRAF3 through the TRAF domain, subsequently decreasing TRAF3 K63-linked ubiquitination. NS1/126-225 binding also disrupted the formation of the mitochondrial antiviral signaling (MAVS)–TRAF3 complex, increasing the recruitment of IKKε to MAVS; ultimately shutting down the RIG-I(N)-mediated signal transduction and cellular antiviral responses. This attenuation of cellular antiviral responses leads to evasion of the innate immune response. Taken together, our findings offer an important insight into the interplay between the influenza virus and host innate immunity.

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“…The crucial role of the IFN response makes it a preferred target for viral evasion. Besides NS1, multiple virus-encoded molecules including the nucleoprotein [ 64 ], the fusion peptide of HA2 (HA2-FP), HA1 and some variants of polymerase subunits PB1-F2, PB1, PB2, PA all counteract the interferon response [ 91 ]. Interestingly, some host cellular molecules are also utilized by IAV to block IFN expression.…”

Section: Immune Evasion By Respiratory Virusesmentioning

confidence: 99%

Immune responses in influenza A virus and human coronavirus infections: an ongoing battle between the virus and host

Zheng

Perlman

2018

Current Opinion in Virology

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Respiratory viruses, especially influenza A viruses and coronaviruses such as MERS-CoV, represent continuing global threats to human health. Despite significant advances, much needs to be learned. Recent studies in virology and immunology have improved our understanding of the role of the immune system in protection and in the pathogenesis of these infections and of co-evolution of viruses and their hosts. These findings, together with sophisticated molecular structure analyses, omics tools and computer-based models, have helped delineate the interaction between respiratory viruses and the host immune system, which will facilitate the development of novel treatment strategies and vaccines with enhanced efficacy.

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To Conquer the Host, Influenza Virus Is Packing It In: Interferon-Antagonistic Strategies beyond NS1

Cited by 18 publications

References 62 publications

How Many Mammalian Reovirus Proteins are involved in the Control of the Interferon Response?

How Many Mammalian Reovirus Proteins are involved in the Control of the Interferon Response?

The C-Terminal Effector Domain of Non-Structural Protein 1 of Influenza A Virus Blocks IFN-β Production by Targeting TNF Receptor-Associated Factor 3

Immune responses in influenza A virus and human coronavirus infections: an ongoing battle between the virus and host

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