scholarly journals Junín Virus Infection Activates the Type I Interferon Pathway in a RIG-I-Dependent Manner

2012 ◽  
Vol 6 (5) ◽  
pp. e1659 ◽  
Author(s):  
Cheng Huang ◽  
Olga A. Kolokoltsova ◽  
Nadezdha E. Yun ◽  
Alexey V. Seregin ◽  
Allison L. Poussard ◽  
...  
Keyword(s):  
Virus Infection ◽  
Type I Interferon ◽  
Type I ◽  
Dependent Manner ◽  
Junin Virus ◽  
Interferon Pathway ◽  
Junín Virus

scholarly journals Author response: Type I interferon underlies severe disease associated with Junín virus infection in mice

2020 ◽  
Author(s):  
Brady T Hickerson ◽  
Eric J Sefing ◽  
Kevin W Bailey ◽  
Arnaud J Van Wettere ◽  
Manuel L Penichet ◽  
...  
Keyword(s):  
Virus Infection ◽  
Type I Interferon ◽  
Severe Disease ◽  
Author Response ◽  
Type I ◽  
Response Type ◽  
Junin Virus ◽  
Junín Virus

scholarly journals Rabies Virus Infection Induces Type I Interferon Production in an IPS-1 Dependent Manner While Dendritic Cell Activation Relies on IFNAR Signaling

2010 ◽  
Vol 6 (7) ◽  
pp. e1001016 ◽  
Author(s):  
Elizabeth J. Faul ◽  
Celestine N. Wanjalla ◽  
Mehul S. Suthar ◽  
Michael Gale ◽  
Christoph Wirblich ◽  
...  
Keyword(s):  
Dendritic Cell ◽  
Virus Infection ◽  
Rabies Virus ◽  
Cell Activation ◽  
Type I Interferon ◽  
Type I ◽  
Dependent Manner ◽  
Interferon Production ◽  
Dendritic Cell Activation ◽  
Rabies Virus Infection

scholarly journals PP2A Facilitates Porcine Reproductive and Respiratory Syndrome Virus Replication by Deactivating irf3 and Limiting Type I Interferon Production

Viruses ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 948 ◽  
Author(s):  
Jiayu Xu ◽  
Lu Zhang ◽  
Yunfei Xu ◽  
He Zhang ◽  
Junxin Gao ◽  
...  
Keyword(s):  
Virus Infection ◽  
Therapeutic Target ◽  
Type I Interferon ◽  
Negative Regulator ◽  
Host Cells ◽  
Respiratory Syndrome Virus ◽  
Target Cells ◽  
Type I ◽  
Dependent Manner ◽  
Pp2a Activity

Protein phosphatase 2A (PP2A), a major serine/threonine phosphatase in mammalian cells, is known to regulate the kinase-driven intracellular signaling pathways. Emerging evidences have shown that the PP2A phosphatase functions as a bona-fide therapeutic target for anticancer therapy, but it is unclear whether PP2A affects a porcine reproductive and respiratory syndrome virus infection. In the present study, we demonstrated for the first time that inhibition of PP2A activity by either inhibitor or small interfering RNA duplexes in target cells significantly reduced their susceptibility to porcine reproductive and respiratory syndrome virus (PRRSV) infection. Further analysis revealed that inhibition of PP2A function resulted in augmented production of type I interferon (IFN). The mechanism is that inhibition of PP2A activity enhances the levels of phosphorylated interferon regulatory factor 3, which activates the transcription of IFN-stimulated genes. Moreover, inhibition of PP2A activity mainly blocked PRRSV replication in the early stage of viral life cycle, after virus entry but before virus release. Using type I IFN receptor 2 specific siRNA in combination with PP2A inhibitor, we confirmed that the effect of PP2A on viral replication within target cells was an interferon-dependent manner. Taken together, these findings demonstrate that PP2A serves as a negative regulator of host cells antiviral responses and provides a novel therapeutic target for virus infection.

scholarly journals DEAD-Box Helicase DDX25 Is a Negative Regulator of Type I Interferon Pathway and Facilitates RNA Virus Infection

2017 ◽  
Vol 7 ◽  
Author(s):  
Tingting Feng ◽  
Ta Sun ◽  
Guanghao Li ◽  
Wen Pan ◽  
Kezhen Wang ◽  
...  
Keyword(s):  
Virus Infection ◽  
Type I Interferon ◽  
Rna Virus ◽  
Negative Regulator ◽  
Type I ◽  
Dead Box ◽  
Interferon Pathway

Differential Expression of the Type I Interferon Pathway during Persistent and Transient Bovine Viral Diarrhea Virus Infection

2009 ◽  
Vol 29 (1) ◽  
pp. 23-36 ◽  
Author(s):  
Megan L. Shoemaker ◽  
Natalia P. Smirnova ◽  
Helle Bielefeldt-Ohmann ◽  
Kathleen J. Austin ◽  
Alberto van Olphen ◽  
...  
Keyword(s):  
Virus Infection ◽  
Differential Expression ◽  
Bovine Viral Diarrhea Virus ◽  
Type I Interferon ◽  
Bovine Viral Diarrhea ◽  
Type I ◽  
Diarrhea Virus ◽  
Viral Diarrhea ◽  
Interferon Pathway ◽  
Viral Diarrhea Virus

scholarly journals Suppression of Type I Interferon Signaling by E1A via RuvBL1/Pontin

2017 ◽  
Vol 91 (8) ◽  
Author(s):  
Oladunni Olanubi ◽  
Jasmine Rae Frost ◽  
Sandi Radko ◽  
Peter Pelka
Keyword(s):  
Gene Expression ◽  
Cellular Response ◽  
Type I Interferon ◽  
Early Gene ◽  
Interferon Response ◽  
Type I ◽  
Dependent Manner ◽  
Interferon Signaling ◽  
Interferon Pathway ◽  
Regulated Promoters

ABSTRACT Suppression of interferon signaling is of paramount importance to a virus. Interferon signaling significantly reduces or halts the ability of a virus to replicate; therefore, viruses have evolved sophisticated mechanisms that suppress activation of the interferon pathway or responsiveness of the infected cell to interferon. Adenovirus has multiple modes of inhibiting the cellular response to interferon. Here, we report that E1A, previously shown to regulate interferon signaling in multiple ways, inhibits interferon-stimulated gene expression by modulating RuvBL1 function. RuvBL1 was previously shown to affect type I interferon signaling. E1A binds to RuvBL1 and is recruited to RuvBL1-regulated promoters in an interferon-dependent manner, preventing their activation. Depletion of RuvBL1 impairs adenovirus growth but does not appear to significantly affect viral protein expression. Although RuvBL1 has been shown to play a role in cell growth, its depletion had no effect on the ability of the virus to replicate its genome or to drive cells into S phase. E1A was found to bind to RuvBL1 via the C terminus of E1A, and this interaction was important for suppression of interferon-stimulated gene transcriptional activation and recruitment of E1A to interferon-regulated promoters. Here, we report the identification of RuvBL1 as a new target for adenovirus in its quest to suppress the interferon response. IMPORTANCE For most viruses, suppression of the interferon signaling pathway is crucial to ensure a successful replicative cycle. Human adenovirus has evolved several different mechanisms that prevent activation of interferon or the ability of the cell to respond to interferon. The viral immediate-early gene E1A was previously shown to affect interferon signaling in several different ways. Here, we report a novel mechanism reliant on RuvBL1 that E1A uses to prevent activation of interferon-stimulated gene expression following infection or interferon treatment. This adds to the growing knowledge of how viruses are able to inhibit interferon and identifies a novel target used by adenovirus for modulation of the cellular interferon pathway.

scholarly journals Bleomycin-Induced Lung Injury Increases Resistance to Influenza Virus Infection in a Type I Interferon-Dependent Manner

2021 ◽  
Vol 12 ◽  
Author(s):  
Sang-Uk Seo ◽  
Jae-Hyeon Jeong ◽  
Bum-Seo Baek ◽  
Je-Min Choi ◽  
Youn Soo Choi ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Virus Infection ◽  
Lung Injury ◽  
Inflammatory Cytokine ◽  
Type I Interferon ◽  
Influenza Infection ◽  
Influenza Virus Infection ◽  
Type I ◽  
Dependent Manner ◽  
Infection Period

Acute lung injury (ALI) results in acute respiratory disease that causes fatal respiratory diseases; however, little is known about the incidence of influenza infection in ALI. Using a ALI-mouse model, we investigated the pro-inflammatory cytokine response to ALI and influenza infection. Mice treated with bleomycin (BLM), which induces ALI, were more resistant to influenza virus infection and exhibited higher levels of type I interferon (IFN-I) transcription during the early infection period than that in PBS-treated control mice. BLM-treated mice also exhibited a lower viral burden, reduced pro-inflammatory cytokine production, and neutrophil levels. In contrast, BLM-treated IFN-I receptor 1 (IFNAR1)-knockout mice failed to show this attenuated phenotype, indicating that IFN-I is key to the antiviral response in ALI-induced mice. The STING/TBK1/IRF3 pathway was found to be involved in IFN-I production and the establishment of an antiviral environment in the lung. The depletion of plasmacytoid dendritic cells (pDCs) reduced the effect of BLM treatment against influenza virus infection, suggesting that pDCs are the major source of IFN-I and are crucial for defense against viral infection in BLM-induced lung injury. Overall, this study showed that BLM-mediated ALI in mice induced the release of double-stranded DNA, which in turn potentiated IFN-I-dependent pulmonary viral resistance by activating the STING/TBK1/IRF3 pathway in association with pDCs.

scholarly journals Junín Virus Infection of Human Hematopoietic Progenitors Impairs In Vitro Proplatelet Formation and Platelet Release via a Bystander Effect Involving Type I IFN Signaling

2010 ◽  
Vol 6 (4) ◽  
pp. e1000847 ◽  
Author(s):  
Roberto G. Pozner ◽  
Agustín E. Ure ◽  
Carolina Jaquenod de Giusti ◽  
Lina P. D'Atri ◽  
Joseph E. Italiano ◽  
...  
Keyword(s):  
Virus Infection ◽  
Bystander Effect ◽  
Type I ◽  
Type I Ifn ◽  
Hematopoietic Progenitors ◽  
Junin Virus ◽  
Platelet Release ◽  
Proplatelet Formation ◽  
Junín Virus

scholarly journals Porcine Epidemic Diarrhea Virus Infection Inhibits Interferon Signaling by Targeted Degradation of STAT1

2016 ◽  
Vol 90 (18) ◽  
pp. 8281-8292 ◽  
Author(s):  
Longjun Guo ◽  
Xiaolei Luo ◽  
Ren Li ◽  
Yunfei Xu ◽  
Jian Zhang ◽  
...  
Keyword(s):  
Virus Infection ◽  
Porcine Epidemic Diarrhea Virus ◽  
Molecular Mechanisms ◽  
Type I Interferon ◽  
Infection Type ◽  
Interferon Response ◽  
Type I ◽  
Dependent Manner ◽  
Diarrhea Virus ◽  
Porcine Epidemic Diarrhea

ABSTRACTPorcine epidemic diarrhea virus (PEDV) is a worldwide-distributed alphacoronavirus, but the pathogenesis of PEDV infection is not fully characterized. During virus infection, type I interferon (IFN) is a key mediator of innate antiviral responses. Most coronaviruses develop some strategy for at least partially circumventing the IFN response by limiting the production of IFN and by delaying the activation of the IFN response. However, the molecular mechanisms by which PEDV antagonizes the antiviral effects of interferon have not been fully characterized. Especially, how PEDV impacts IFN signaling components has yet to be elucidated. In this study, we observed that PEDV was relatively resistant to treatment with type I IFN. Western blot analysis showed that STAT1 expression was markedly reduced in PEDV-infected cells and that this reduction was not due to inhibition of STAT1 transcription. STAT1 downregulation was blocked by a proteasome inhibitor but not by an autophagy inhibitor, strongly implicating the ubiquitin-proteasome targeting degradation system. Since PEDV infection-induced STAT1 degradation was evident in cells pretreated with the general tyrosine kinase inhibitor, we conclude that STAT1 degradation is independent of the IFN signaling pathway. Furthermore, we report that PEDV-induced STAT1 degradation inhibits IFN-α signal transduction pathways. Pharmacological inhibition of STAT1 degradation rescued the ability of the host to suppress virus replication. Collectively, these data show that PEDV is capable of subverting the type I interferon response by inducing STAT1 degradation.IMPORTANCEIn this study, we show that PEDV is resistant to the antiviral effect of IFN. The molecular mechanism is the degradation of STAT1 by PEDV infection in a proteasome-dependent manner. This PEDV infection-induced STAT1 degradation contributes to PEDV replication. Our findings reveal a new mechanism evolved by PEDV to circumvent the host antiviral response.

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