scholarly journals The VP3 Protein of Bluetongue Virus Associates with the MAVS Complex and Interferes with the RIG-I-Signaling Pathway

Viruses ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 230
Author(s):  
Marie Pourcelot ◽  
Rayane Amaral Moraes ◽  
Aurore Fablet ◽  
Emmanuel Bréard ◽  
Corinne Sailleau ◽  
...  
Keyword(s):  
Bluetongue Virus ◽  
Type I Interferon ◽  
Type I ◽  
Adapter Protein ◽  
Structural Protein ◽  
Innate Response ◽  
Biting Midges ◽  
Domestic Ruminants ◽  
Infected Cells ◽  
Culicoides Biting Midges

Bluetongue virus (BTV), an arbovirus transmitted by Culicoides biting midges, is a major concern of wild and domestic ruminants. While BTV induces type I interferon (alpha/beta interferon [IFN-α/β]) production in infected cells, several reports have described evasion strategies elaborated by this virus to dampen this intrinsic, innate response. In the present study, we suggest that BTV VP3 is a new viral antagonist of the IFN-β synthesis. Indeed, using split luciferase and coprecipitation assays, we report an interaction between VP3 and both the mitochondrial adapter protein MAVS and the IRF3-kinase IKKε. Overall, this study describes a putative role for the BTV structural protein VP3 in the control of the antiviral response.

scholarly journals Retrospective Analysis of the Bluetongue Outbreak in Serbia

2017 ◽  
Vol 40 (1) ◽  
pp. 21-27 ◽  
Author(s):  
Spomenka Djurić ◽  
Predrag Simeunović ◽  
Milorad Mirilović ◽  
Jevrosima Stevanović ◽  
Uroš Glavinić ◽  
...  
Keyword(s):  
Bluetongue Virus ◽  
Control Measure ◽  
Infected Sheep ◽  
Economic Losses ◽  
Biting Midges ◽  
Domestic Ruminants ◽  
Investigation Period ◽  
Bluetongue Disease ◽  
Culicoides Biting Midges ◽  
Veterinary Institute

Abstract Bluetongue, a vector-born disease caused by the Bluetongue virus (BTV) and transmitted by Culicoides biting midges, is considered to be one of the most important diseases of domestic ruminants. The first outbreak of bluetongue in Serbia was reported in 2001, when BTV serotype 9 was identified in sampled materials. In 2014, outbreak of BTV-4 in Serbia caused considerable economic losses affecting sheep, cattle and goats. During this outbreak, BTV-4 was recorded in 644 outbreaks within 49 municipalities, part of 17 administrative regions. From the total number of sheep kept in areas affected by bluetongue (n=1 748 110), 2 083 cases (0.2%) were proven to be BTV-4 infected. Total of 206 infected cattle and 24 infected goats were reported during this investigation period, which represents 0.06% and 0.03% of the total number of cattle and goats kept in affected areas, respectively. The highest incidence of infected sheep, cattle and goats was recorded on the territory covered by veterinary institute of Nis. Recorded lethality in cattle, sheep and goats was 18.45% (n=38), 48.10% (n=1002) and 54.17% (n=13), respectively. The peak of the outbreak was in September and October when 94.43% of the confirmed positive cases, regardless of the species, was recorded. Monitoring of bluetongue disease in Serbia relies on active surveillance programmes aimed at: (i) identification and tracing of susceptible and potentially infected animals and (ii) detection, distribution and prevalence of insect vectors. Vaccination of sheep is planned to be implemented as a control measure against bluetongue in Serbia.

The CrkL Adapter Protein Is Required for Type I Interferon-Dependent Gene Transcription and Activation of the Small G-Protein Rap1

2002 ◽  
Vol 291 (4) ◽  
pp. 744-750 ◽  
Author(s):  
Fatima Lekmine ◽  
Antonella Sassano ◽  
Shahab Uddin ◽  
Beata Majchrzak ◽  
Osamu Miura ◽  
...  
Keyword(s):  
G Protein ◽  
Gene Transcription ◽  
Type I Interferon ◽  
Type I ◽  
Adapter Protein ◽  
Small G Protein

scholarly journals Measurement of the Infection and Dissemination of Bluetongue Virus in Culicoides Biting Midges Using a Semi-Quantitative RT-PCR Assay and Isolation of Infectious Virus

PLoS ONE ◽  
2013 ◽  
Vol 8 (8) ◽  
pp. e70800 ◽  
Author(s):  
Eva Veronesi ◽  
Frank Antony ◽  
Simon Gubbins ◽  
Nick Golding ◽  
Alison Blackwell ◽  
...  
Keyword(s):  
Bluetongue Virus ◽  
Infectious Virus ◽  
Rt Pcr ◽  
Pcr Assay ◽  
Biting Midges ◽  
Culicoides Biting Midges

scholarly journals Lys29-linkage of ASK1 by Skp1−Cullin 1−Fbxo21 ubiquitin ligase complex is required for antiviral innate response

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Zhou Yu ◽  
Taoyong Chen ◽  
Xuelian Li ◽  
Mingjin Yang ◽  
Songqing Tang ◽  
...  
Keyword(s):  
Ubiquitin Ligase ◽  
Type I Interferon ◽  
Innate Immune ◽  
Type I ◽  
Innate Response ◽  
Scf Complex ◽  
Protein Ubiquitination ◽  
Ubiquitin Ligase Complex ◽  
F Box Protein ◽  
Unknown Component

Protein ubiquitination regulated by ubiquitin ligases plays important roles in innate immunity. However, key regulators of ubiquitination during innate response and roles of new types of ubiquitination (apart from Lys48- and Lys63-linkage) in control of innate signaling have not been clearly understood. Here we report that F-box only protein Fbxo21, a functionally unknown component of SCF (Skp1–Cul1–F-box protein) complex, facilitates Lys29-linkage and activation of ASK1 (apoptosis signal-regulating kinase 1), and promotes type I interferon production upon viral infection. Fbxo21 deficiency in mice cells impairs virus-induced Lys29-linkage and activation of ASK1, attenuates c-Jun N-terminal kinase (JNK) and p38 signaling pathway, and decreases the production of proinflammatory cytokines and type I interferon, resulting in reduced antiviral innate response and enhanced virus replication. Therefore Fbxo21 is required for ASK1 activation via Lys29-linkage of ASK1 during antiviral innate response, providing mechanistic insights into non-proteolytic roles of SCF complex in innate immune response.

scholarly journals Induction and control of the type I interferon pathway by Bluetongue virus

2014 ◽  
Vol 182 ◽  
pp. 59-70 ◽  
Author(s):  
Damien Vitour ◽  
Virginie Doceul ◽  
Suzana Ruscanu ◽  
Emilie Chauveau ◽  
Isabelle Schwartz-Cornil ◽  
...  
Keyword(s):  
Bluetongue Virus ◽  
Type I Interferon ◽  
Type I ◽  
Interferon Pathway ◽  
And Control

scholarly journals Efficient dengue virus (DENV) infection of human muscle satellite cells upregulates type I interferon response genes and differentially modulates MHC I expression on bystander and DENV-infected cells

2008 ◽  
Vol 89 (7) ◽  
pp. 1605-1615 ◽  
Author(s):  
Rajas V. Warke ◽  
Aniuska Becerra ◽  
Agatha Zawadzka ◽  
Diane J. Schmidt ◽  
Katherine J. Martin ◽  
...  
Keyword(s):  
Cell Surface ◽  
Satellite Cells ◽  
Culture Medium ◽  
Type I Interferon ◽  
Denv Infection ◽  
Human Muscle ◽  
Type I ◽  
Mhc I ◽  
Muscle Satellite Cells ◽  
Infected Cells

Dengue virus (DENV) is a mosquito-borne flavivirus that causes an acute febrile disease in humans, characterized by musculoskeletal pain, headache, rash and leukopenia. The cause of myalgia during DENV infection is still unknown. To determine whether DENV can infect primary muscle cells, human muscle satellite cells were exposed to DENV in vitro. The results demonstrated for the first time high-efficiency infection and replication of DENV in human primary muscle satellite cells. Changes in global gene expression were also examined in these cells following DENV infection using Affymetrix GeneChip analysis. The differentially regulated genes belonged to two main functional categories: cell growth and development, and antiviral type I interferon (IFN) response genes. Increased expression of the type I IFN response genes for tumour necrosis factor-related apoptosis-inducing ligand (TRAIL), melanoma-derived antigen 5 (MDA-5), IFN-γ-inducible protein 10 (IP-10), galectin 3 soluble binding protein (LGals3BP) and IFN response factor 7 (IRF7) was confirmed by quantitative RT-PCR. Furthermore, higher levels of cell-surface-bound intracellular adhesion molecule-1 (ICAM-1) and soluble ICAM-1 in the cell-culture medium were detected following DENV infection. However, DENV infection impaired the ability of the infected cells in the culture medium to upregulate cell-surface expression of MHC I molecules, suggesting a possible mechanism of immune evasion by DENV. The findings of this study warrant further clinical research to identify whether muscle cells are targets for DENV infection during the acute stage of the disease in vivo.

scholarly journals NS3 of Bluetongue Virus Interferes with the Induction of Type I Interferon

2013 ◽  
Vol 87 (14) ◽  
pp. 8241-8246 ◽  
Author(s):  
E. Chauveau ◽  
V. Doceul ◽  
E. Lara ◽  
E. Breard ◽  
C. Sailleau ◽  
...  
Keyword(s):  
Bluetongue Virus ◽  
Type I Interferon ◽  
Type I

scholarly journals SARS-CoV-2 non-structural protein 1 inhibits the interferon response by causing depletion of key host signaling factors.

2021 ◽  
Author(s):  
Anil Kumar ◽  
Ray Ishida ◽  
Tania Strilets ◽  
Jamie Cole ◽  
Joaquin Lopez-Orozco ◽  
...  
Keyword(s):  
Causative Agent ◽  
Interferon Response ◽  
Type I ◽  
Structural Protein ◽  
Type I Ifns ◽  
Rapid Spread ◽  
Host Signaling ◽  
Infected Cells ◽  
Serious Disease ◽  
Taste And Smell

Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is the causative agent of the ongoing COVID-19 pandemic. While previous studies have shown that several SARS-CoV-2 proteins can antagonize the interferon (IFN) response, some of the mechanisms by which they do so are not well understood. In this study, we describe two novel mechanisms by which SARS-CoV-2 blocks the IFN pathway. Type I IFNs and IFN-stimulated genes (ISGs) were poorly induced during SARS-CoV-2 infection and once infection was established, cells were highly resistant to ectopic induction of IFNs and ISGs. Levels of two key IFN signaling pathway components, Tyk2 and STAT2 were significantly lower in SARS-CoV-2 infected cells. Expression of non-structural protein 1 (NSP1) or nucleocapsid in the absence of other viral proteins was sufficient to block IFN induction but only NSP1 was able to inhibit IFN signaling. Mapping studies suggest that NSP1 prevents IFN induction in part by blocking IRF3 phosphorylation. In addition, NSP1-induced depletion of Tyk2 and STAT2 dampened ISG induction. Together, our study provides new insights into how SARS-CoV-2 successfully evades the IFN system to establish infection. Importance SARS-CoV-2 is the causative agent of COVID-19, a serious disease that can have myriad of symptoms from loss of taste and smell to pneumonia and hypercoagulation. The rapid spread of SARS-CoV-2 can be attributed in part to asymptomatic transmission, where infected individuals shed large amounts of virus before the onset of disease. This is likely due to the ability of SARS-CoV-2 to effectively suppress the innate immune system, including the IFN response. Indeed, we show that the IFN response is efficiently blocked during SARS-CoV-2 infection, a process that is mediated in large part by non-structural protein 1 and nucleocapsid. Our study provides new insights on how SARS-CoV-2 evades the IFN response to successfully establish infection. These findings should be considered for the development and administration of therapeutics against SARS-CoV-2.

Transcriptome analysis of senecavirus A-infected cells: Type I interferon is a critical anti-viral factor

2020 ◽  
Vol 147 ◽  
pp. 104432
Author(s):  
Jing Wang ◽  
Chunxiao Mou ◽  
Minmin Wang ◽  
Shuonan Pan ◽  
Zhenhai Chen
Keyword(s):  
Transcriptome Analysis ◽  
Type I Interferon ◽  
Type I ◽  
Viral Factor ◽  
Infected Cells

scholarly journals Epstein-Barr Virus (EBV) Tegument Protein BGLF2 Suppresses Type I Interferon Signaling To Promote EBV Reactivation

2020 ◽  
Vol 94 (11) ◽  
Author(s):  
XueQiao Liu ◽  
Tomohiko Sadaoka ◽  
Tammy Krogmann ◽  
Jeffrey I. Cohen
Keyword(s):  
Virus Infection ◽  
Type I Interferon ◽  
Tegument Protein ◽  
Type I ◽  
Type I Ifn ◽  
Virus Reactivation ◽  
Ebv Infection ◽  
Ebv Reactivation ◽  
Stat3 Phosphorylation ◽  
Infected Cells

ABSTRACT Interferon alpha (IFN-α) and IFN-β are type I IFNs that are induced by virus infection and are important in the host’s innate antiviral response. EBV infection activates multiple cell signaling pathways, resulting in the production of type I IFN which inhibits EBV infection and virus-induced B-cell transformation. We reported previously that EBV tegument protein BGLF2 activates p38 and enhances EBV reactivation. To further understand the role of BGLF2 in EBV infection, we used mass spectrometry to identify cellular proteins that interact with BGLF2. We found that BGLF2 binds to Tyk2 and confirmed this interaction by coimmunoprecipitation. BGLF2 blocked type I IFN-induced Tyk2, STAT1, and STAT3 phosphorylation and the expression of IFN-stimulated genes (ISGs) IRF1, IRF7, and MxA. In contrast, BGLF2 did not inhibit STAT1 phosphorylation induced by IFN-γ. Deletion of the carboxyl-terminal 66 amino acids of BGLF2 reduced the ability of the protein to repress type I IFN signaling. Treatment of gastric carcinoma and Raji cells with IFN-α blocked BZLF1 expression and EBV reactivation; however, expression of BGLF2 reduced the ability of IFN-α to inhibit BZLF1 expression and enhanced EBV reactivation. In summary, EBV BGLF2 interacts with Tyk2, inhibiting Tyk2, STAT1, and STAT3 phosphorylation and impairs type I IFN signaling; BGLF2 also counteracts the ability of IFN-α to suppress EBV reactivation. IMPORTANCE Type I interferons are important for controlling virus infection. We have found that the Epstein-Barr virus (EBV) BGLF2 tegument protein binds to a protein in the type I interferon signaling pathway Tyk2 and inhibits the expression of genes induced by type I interferons. Treatment of EBV-infected cells with type I interferon inhibits reactivation of the virus, while expression of EBV BGLF2 reduces the ability of type I interferon to inhibit virus reactivation. Thus, a tegument protein delivered to cells during virus infection inhibits the host’s antiviral response and promotes virus reactivation of latently infected cells. Therefore, EBV BGLF2 might protect virus-infected cells from the type I interferon response in cells undergoing lytic virus replication.

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