Robust Lys63-Linked Ubiquitination of RIG-I Promotes Cytokine Eruption in Early Influenza B Virus Infection

Jiang, Jingwen; Li, Jing; Fan, Wenhui; Zheng, Wei; Yu, Meng; Chen, Can; Sun, Lei; Bi, Yuhai; Ding, Chan; Gao, George F.; Liu, Wenjun

doi:10.1128/jvi.00549-16

Cited by 27 publications

(26 citation statements)

References 52 publications

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“…Phosphorylation of another site on NS1, Thr80, has also been reported to disrupt NS1 binding affinity with RIG-I (103). Similar to IAV, the IBV non-structural NS protein (NS1-B) has recently been described as inhibiting RIG-I ubiquitination, which involves TRIM25-NS1 C-terminal effector domain interaction and the RIG-I/TRIM25/ NS1-B complex formation (104). By contrast, the protease NS3-4A of HCV functions differently, rather than inhibiting TRIM25, it is thought to target the E3 ligase Riplet.…”

Section: Modulation Of the Ptmsmentioning

confidence: 99%

Host and Viral Modulation of RIG-I-Mediated Antiviral Immunity

2017

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Innate immunity is the first line of defense against invading pathogens. Rapid and efficient detection of pathogen-associated molecular patterns via pattern-recognition receptors is essential for the host to mount defensive and protective responses. Retinoic acid-inducible gene-I (RIG-I) is critical in triggering antiviral and inflammatory responses for the control of viral replication in response to cytoplasmic virus-specific RNA structures. Upon viral RNA recognition, RIG-I recruits the mitochondrial adaptor protein mitochondrial antiviral signaling protein, which leads to a signaling cascade that coordinates the induction of type I interferons (IFNs), as well as a large variety of antiviral interferon-stimulated genes. The RIG-I activation is tightly regulated via various posttranslational modifications for the prevention of aberrant innate immune signaling. By contrast, viruses have evolved mechanisms of evasion, such as sequestrating viral structures from RIG-I detections and targeting receptor or signaling molecules for degradation. These virus–host interactions have broadened our understanding of viral pathogenesis and provided insights into the function of the RIG-I pathway. In this review, we summarize the recent advances regarding RIG-I pathogen recognition and signaling transduction, cell-intrinsic control of RIG-I activation, and the viral antagonism of RIG-I signaling.

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Section: Modulation Of the Ptmsmentioning

confidence: 99%

Host and Viral Modulation of RIG-I-Mediated Antiviral Immunity

2017

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“…FLUBV undergoes uncoating after fusion of viral and endosomal membranes, but many of the details of FLUBV uptake and uncoating are still unknown. Interestingly, cellular immune responses to FLUBV infection differ from those to FLUAV infection (Jiang et al, 2016;Mäkelä et al, 2015). Therefore, it is possible that host processes involved in other steps of FLUBV infection also differ, as suggested by the discordant importance of EPS8 for FLUAV and FLUBV.…”

Section: Discussionmentioning

confidence: 99%

EPS8 facilitates uncoating of influenza A virus

Larson

Tran

Yú

et al. 2019

Preprint

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All viruses balance interactions between cellular machinery co-opted to support replication and host factors deployed to halt the infection. We used gene correlation analysis to perform an unbiased screen for host factors involved in influenza A virus (FLUAV) infection. Our screen identified the cellular factor epidermal growth factor receptor pathway substrate 8 (EPS8) as the highest confidence pro-viral candidate. Knockout and overexpression of EPS8 confirmed its importance in enhancing FLUAV infection and titers. Loss of EPS8 did not affect virion attachment, uptake, or fusion. Rather, our data show that EPS8 specifically functions during virion uncoating. EPS8 physically associated with incoming virion components, and subsequent nuclear import of released ribonucleoprotein complexes was significantly delayed in the absence of EPS8. Our study identified EPS8 as a host factor important for uncoating, a crucial step of FLUAV infection during which the interface between the virus and host is still being discovered.

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“…During the infection, viruses are recognized by pattern recognition receptors, the innate response is triggered, and interferons (IFNs) are secreted to limit early viral proliferation [6]. This identification leads to an appropriate antiviral response and to the activation of inflammatory response and adaptive immune responses [7]. While the reasons for the limited host range of IBV remain unclear, one of explanations is that the interaction between IBV and the innate immune system imbues the virus with distinct characteristics, such as the role of ISG15, a typical interferon-induced antiviral gene for the innate immune response [8,9].…”

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confidence: 99%

“…Existing studies describe the production of host cytokines, including IFNs, IFN-stimulated genes (ISGs), and proinflammatory cytokines against influenza virus infection, as integral parts of the process of the cellular antiviral response [10][11][12][13]. We have also reported that type I IFNs, ISGs, and proinflammatory cytokines can be induced by IBV virions at the early stage of virus infection [7,14].The interaction between influenza virus infection and the host anti-viral response has been investigated in depth [15,16], and the regulatory mechanism of IBV infection is also under investigation. Previous research has already shown that IBV ribonucleoprotein rapidly activates TLR signaling pathways [14].…”

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Robust induction of interferon and interferon-stimulated gene expression by influenza B/Yamagata lineage virus infection of A549 cells

et al. 2020

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Influenza B virus (IBV) belongs to the Orthomyxoviridae family and generally causes sporadic epidemics but is occasionally deadly to individuals. The current research mainly focuses on clinical and pathological characteristics of IBV. However, to better prevent or treat the disease, one must determine the strategies developed by IBV to invade and disrupt cellular proteins and approach to replicate itself, to suppress antiviral innate immunity, and understand how the host responds to IBV infection. The B/Shanghai/PD114/2018 virus was able to infect alveolar epithelial cells (A549) cells, with good potential for replication. To identify host cellular responses against IBV infection, differentially expressed genes (DEGs) were obtained using RNA sequencing. The GO and KEGG pathway term enrichment analyses with the DEGs were performed, and we found that the DEGs were primary involved in metabolic processes and cellular function, which may be related to the host response, including the innate immune response against the virus. Our transcriptome analysis results demonstrated robust induction of interferon and interferon-stimulated gene expression by IBV in human cells during the early stages of infection, providing a foundation for further studies focused on antiviral drug development and interactions between the virus and host. OPEN ACCESS Citation: Jiao P, Fan W, Cao Y, Zhang H, Tian L, Sun L, et al. (2020) Robust induction of interferon and interferon-stimulated gene expression by influenza B/Yamagata lineage virus infection of A549 cells. PLoS ONE 15(4): e0231039. https://rate is slower compared with influenza A viruses [4]. IBV is a pathogen with very limited host range, and its natural host is mainly humans with fever and cold symptoms. However, seasonal pandemics can break out, such as from the winter of 2017 to the spring of 2018, when the Yamagata lineage strain became the dominant pandemic strain alongside IAV (H1N1 and H3N2) [5].When influenza virus invades a host cell, the innate immune system is activated against the virus. During the infection, viruses are recognized by pattern recognition receptors, the innate response is triggered, and interferons (IFNs) are secreted to limit early viral proliferation [6]. This identification leads to an appropriate antiviral response and to the activation of inflammatory response and adaptive immune responses [7]. While the reasons for the limited host range of IBV remain unclear, one of explanations is that the interaction between IBV and the innate immune system imbues the virus with distinct characteristics, such as the role of ISG15, a typical interferon-induced antiviral gene for the innate immune response [8,9]. Existing studies describe the production of host cytokines, including IFNs, IFN-stimulated genes (ISGs), and proinflammatory cytokines against influenza virus infection, as integral parts of the process of the cellular antiviral response [10][11][12][13]. We have also reported that type I IFNs, ISGs, and proinflammatory cytokines can be induced by IBV viri...

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Robust Lys63-Linked Ubiquitination of RIG-I Promotes Cytokine Eruption in Early Influenza B Virus Infection

Abstract: Influenza

Cited by 27 publications

References 52 publications

Host and Viral Modulation of RIG-I-Mediated Antiviral Immunity

Host and Viral Modulation of RIG-I-Mediated Antiviral Immunity

EPS8 facilitates uncoating of influenza A virus

Robust induction of interferon and interferon-stimulated gene expression by influenza B/Yamagata lineage virus infection of A549 cells

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