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[PMID]:28827284
[Au] Autor:Song DJ; Miller M; Beppu A; Rosenthal P; Das S; Karta M; Vuong C; Mehta AK; Croft M; Broide DH
[Ad] Endereço:Department of Medicine, University of California, San Diego, La Jolla, CA 92093.
[Ti] Título:Rhinovirus Infection of ORMDL3 Transgenic Mice Is Associated with Reduced Rhinovirus Viral Load and Airway Inflammation.
[So] Source:J Immunol;199(7):2215-2224, 2017 Oct 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Orosomucoid like 3 (ORMDL3), a gene localized to chromosome 17q21, has been linked in epidemiologic studies to childhood asthma and rhinovirus (RV) infections. As the single nucleotide polymorphisms linking ORMDL3 to asthma are associated with increased expression of ORMDL3, we have used hORMDL3 mice (which have universal increased expression of human ORMDL3) to determine whether infection of these transgenic mice with RV influences levels of airway inflammation or RV viral load. RV infection of hORMDL3 mice resulted in reduced RV viral load assessed by quantitative real-time PCR (lung and airway epithelium), as well as reduced airway inflammation (total bronchoalveolar lavage cells, neutrophils, macrophages, and lymphocytes) compared with RV-infected wild-type mice. Levels of the antiviral pathways including IFNs (IFN-α, IFN-ß, IFN-λ) and RNAse L were significantly increased in the lungs of RV-infected hORMDL3 mice. Levels of the antiviral mouse oligoadenylate synthetase (mOas)1g pathway and RNAse L were upregulated in the lungs of unchallenged hORMDL3 mice. In addition, levels of mOas2, but not mOas1 (mOas1a, mOas1b, mOas1g), or mOas3 pathways were significantly more upregulated by IFNs (IFN-α, IFN-ß, IFN-λ) in epithelial cells from hORMDL3 mice compared with RV-infected wild-type mouse epithelial cells. RNAse L-deficient mice infected with RV had increased RV viral load. Overall, these studies suggest that increased levels of ORMDL3 contribute to antiviral defense to RV infection in mice through pathways that may include IFNs (IFN-α, IFN-ß, IFN-λ), OAS, and RNAse L.
[Mh] Termos MeSH primário: Pulmão/virologia
Proteínas de Membrana/genética
Proteínas de Membrana/metabolismo
Infecções por Picornaviridae/imunologia
Infecções por Picornaviridae/virologia
Rhinovirus/isolamento & purificação
[Mh] Termos MeSH secundário: 2',5'-Oligoadenilato Sintetase/genética
2',5'-Oligoadenilato Sintetase/metabolismo
Animais
Asma/imunologia
Asma/virologia
Endorribonucleases/deficiência
Endorribonucleases/genética
Endorribonucleases/metabolismo
Células Epiteliais/virologia
Inflamação/imunologia
Inflamação/virologia
Interferon beta/biossíntese
Interferon beta/genética
Interferon beta/imunologia
Interferons/biossíntese
Interferons/genética
Interferons/imunologia
Pulmão/imunologia
Camundongos
Camundongos Transgênicos
Infecções por Picornaviridae/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Carga Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Membrane Proteins); 0 (ORMDL3 protein, human); 77238-31-4 (Interferon-beta); 9008-11-1 (Interferons); EC 2.7.7.- (Oasl1 protein, mouse); EC 2.7.7.84 (2',5'-Oligoadenylate Synthetase); EC 3.1.- (Endoribonucleases); EC 3.1.26.- (2-5A-dependent ribonuclease)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170823
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601412


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[PMID]:28754636
[Au] Autor:Bi KR; Han KK; Liu QT; Zhao DM; Huang XM; Liu YZ; Yang J; Li Y
[Ad] Endereço:Key Laboratory of Veterinary Biological Engineering and Technology, National Center for Engineering Research of Veterinary Bio-products, Institute of Veterinary Medicine, Ministry of Agriculture, Jiangsu Academy of Agricultural Sciences, Nanjing, China; Jiangsu Key Laboratory for Marine Biotechnolog
[Ti] Título:Molecular cloning, characterization, and expression of duck 2'-5'-oligoadenylate synthetase-like gene.
[So] Source:Gene;629:43-51, 2017 Sep 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:2'-5'-Oligoadenylate synthetase-like protein (OASL) is an interferon-inducible antiviral protein that exerts antiviral effects through the RNase L- or retinoic acid-inducible gene I (RIG-I)-dependent signalling pathway. In this study, we identified and cloned the OASL gene (named duOASL) from healthy adult Cherry Valley ducks. Full-length duOASL cDNA (1630bp) encoded a 504-amino acid polypeptide containing three conserved domains, namely, nucleotidyltransferase domain, 2'-5'-oligoadenylate synthetase domain, and two ubiquitin-like repeats. DuOASL mRNA expression was quantified by performing quantitative reverse transcription-PCR (qRT-PCR). Results of qRT-PCR showed that duOASL was broadly expressed in all examined tissues, with the highest mRNA expression in the large intestine. Antiviral activity of duOASL was measured by determining its effect on Duck Tembusu virus (DTMUV) replication in vitro. We found that duOASL overexpression slightly inhibited DTMUV replication, whereas duOASL knockdown by using a specific small interfering RNA increased DTMUV replication in DF-1 cells. Thus, we successfully cloned and characterized the antiviral protein duOASL from Cherry Valley ducks and found that it exerted antiviral effects against DTMUV. These results provide a solid foundation for performing further studies to determine the mechanism underlying the antiviral effect of duOASL at the cellular level.
[Mh] Termos MeSH primário: 2´,5´-Oligoadenilato Sintetase/genética
Proteínas Aviárias/genética
Clonagem Molecular
Patos/genética
Flavivirus/imunologia
[Mh] Termos MeSH secundário: 2',5'-Oligoadenilato Sintetase/análise
2',5'-Oligoadenilato Sintetase/química
2',5'-Oligoadenilato Sintetase/imunologia
Sequência de Aminoácidos
Animais
Proteínas Aviárias/análise
Proteínas Aviárias/química
Proteínas Aviárias/imunologia
Flavivirus/classificação
Especificidade de Órgãos
Filogenia
Alinhamento de Sequência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Avian Proteins); EC 2.7.7.84 (2',5'-Oligoadenylate Synthetase)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170730
[St] Status:MEDLINE


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[PMID]:28724761
[Au] Autor:Sooryanarain H; Rogers AJ; Cao D; Haac MER; Karpe YA; Meng XJ
[Ad] Endereço:Department of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Blacksburg, Virginia, USA.
[Ti] Título:ISG15 Modulates Type I Interferon Signaling and the Antiviral Response during Hepatitis E Virus Replication.
[So] Source:J Virol;91(19), 2017 Oct 01.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hepatitis E virus (HEV), a single-stranded positive-sense RNA virus, generally causes self-limiting acute viral hepatitis, although chronic HEV infection has recently become a significant clinical problem in immunocompromised individuals, especially in solid-organ transplant recipients. Innate immunity, via the type I interferon (IFN) response, plays an important role during the initial stages of a viral infection. IFN-stimulated gene 15 (ISG15), an IFN-induced ubiquitin-like protein, is known to have an immunomodulatory role and can have a direct antiviral effect on a wide spectrum of virus families. In the present study, we investigated the antiviral effect as well as the potential immunomodulatory role of ISG15 during HEV replication. The results revealed that HEV induced high levels of ISG15 production both (Huh7-S10-3 liver cells) and (liver tissues from HEV-infected pigs); however, ISG15 is not required for virus replication. We also demonstrated that ISG15 silencing potentiates enhanced type I IFN-mediated signaling, resulting in an increase in the type I IFN-mediated antiviral effect during HEV replication. This observed enhanced type I IFN signaling correlated with an increase in IFN-stimulated gene expression levels during HEV replication. Furthermore, we showed that PKR and OAS1 played important roles in the ISG15-mediated type I IFN sensitivity of HEV. Taken together, the results from this study suggest that ISG15 plays an important immunomodulatory role and regulates HEV sensitivity to exogenous type I IFN. Hepatitis E virus (HEV) infection typically causes self-limiting acute viral hepatitis. However, chronic HEV infection has recently become a significant clinical problem in immunocompromised patients. Pegylated interferon (IFN) has been used to treat chronic HEV infection in solid-organ transplant patients with some success. However, the mechanism behind the type I IFN-mediated antiviral effect against HEV remains unclear. This report demonstrates that ISG15 induced by HEV replication in Huh7-S10-3 human liver cells plays an immunomodulatory role by negatively regulating type I IFN signaling and, thus, HEV sensitivity to type I IFN. Our results also show that PKR and OAS1 play important roles in the ISG15-mediated type I IFN sensitivity of HEV.
[Mh] Termos MeSH primário: Citocinas/imunologia
Vírus da Hepatite E/crescimento & desenvolvimento
Hepatite E/imunologia
Interferon-alfa/imunologia
Ubiquitinas/imunologia
Replicação Viral/imunologia
[Mh] Termos MeSH secundário: 2',5'-Oligoadenilato Sintetase/metabolismo
Animais
Linhagem Celular Tumoral
Citocinas/genética
Hepatite E/virologia
Vírus da Hepatite E/genética
Vírus da Hepatite E/imunologia
Hepatócitos/imunologia
Hepatócitos/virologia
Seres Humanos
Interferência de RNA
RNA Interferente Pequeno/genética
Transdução de Sinais/imunologia
Suínos
Ubiquitinas/genética
Replicação Viral/genética
eIF-2 Quinase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Interferon-alpha); 0 (RNA, Small Interfering); 0 (Ubiquitins); 60267-61-0 (ISG15 protein, human); EC 2.7.11.1 (EIF2AK2 protein, human); EC 2.7.11.1 (eIF-2 Kinase); EC 2.7.7.- (OAS1 protein, human); EC 2.7.7.84 (2',5'-Oligoadenylate Synthetase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170721
[St] Status:MEDLINE


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[PMID]:28704535
[Au] Autor:López-Rodríguez R; Hernández-Bartolomé Á; Borque MJ; Rodríguez-Muñoz Y; Martín-Vílchez S; García-Buey L; González-Moreno L; Real-Martínez Y; Muñoz de Rueda P; Salmerón J; Vidal-Castiñeira JR; López-Larrea C; Rodrigo L; Moreno-Otero R; Sanz-Cameno P
[Ad] Endereço:Liver Unit, Gastroenterology Service, Instituto Investigación Sanitaria Princesa, IIS-IP, Madrid, Spain.
[Ti] Título:Interferon-related genetic markers of necroinflammatory activity in chronic hepatitis C.
[So] Source:PLoS One;12(7):e0180927, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Chronic hepatitis C (CHC) is a major cause of liver disease worldwide which often leads to progressive liver inflammation, fibrosis, cirrhosis and hepatocellular carcinoma (HCC). CHC displays heterogeneous progression depending on a broad set of factors, some of them intrinsic to each individual such as the patient's genetic profile. This study aims to evaluate the contribution of certain genetic variants of crucial interferon alpha and lambda signaling pathways to the hepatic necroinflammatory activity (NIA) grade of CHC patients. METHODS: NIA was evaluated in 119 CHC patients by METAVIR scale and classified as low (NIA = 0-2, n = 80) or high grade (NIA = 3, n = 39). In a candidate gene approach, 64 SNPs located in 30 different genes related to interferon pathways (IL-28B, IFNAR1-2, JAK-STAT and OAS1-3, among others) were genotyped using the Illumina GoldenGate® Genotyping Assay. Statistical association was determined by logistic regression and expressed as OR and 95% CI. Those SNPs significantly associated were further adjusted by other covariates. RESULTS: Seven SNPs located in IL-28B (rs12979860), JAK1 (rs11576173 and rs1497056), TYK2 (rs280519), OAS1 (rs2057778), SOCS1 (rs33932899) and RNASEL (rs3738579) genes were significantly related to severe NIA grade (p<0.05). Regarding to clinical variables, elevated NIA was notably associated with aspartate aminotransferase (AST) serum levels >40 IU/L (p<0.05) but not with other clinical factors. Multivariate logistic regression analysis of these factors reflected that AST (>40 IU/L), TYK2 rs280519 (G allele) and RNASEL rs3738579 (G allele) were factors independently associated with elevated NIA (p<0.05). AST concentration showed a moderate AUC value (AUC = 0.63), similar to TYK2 (rs280519) and RNASEL (rs3738579) SNPs (AUC = 0.61, both) in the ROC_AUC analysis. Interestingly, the model including all significant variables reached a considerable predictive value (AUC = 0.74). CONCLUSION: The identified genetic variants in interferon signaling pathways may constitute useful prognostic markers of CHC progression. Further validation in larger cohorts of patients is needed.
[Mh] Termos MeSH primário: Hepatite C Crônica/genética
Interleucinas/genética
Polimorfismo de Nucleotídeo Único
[Mh] Termos MeSH secundário: 2',5'-Oligoadenilato Sintetase/genética
Adulto
Idoso
Aspartato Aminotransferases/sangue
Endorribonucleases/genética
Feminino
Hepatite C Crônica/sangue
Hepatite C Crônica/patologia
Seres Humanos
Janus Quinase 1/genética
Masculino
Meia-Idade
Proteína 1 Supressora da Sinalização de Citocina/genética
TYK2 Quinase/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IL28B protein, human); 0 (Interleukins); 0 (SOCS1 protein, human); 0 (Suppressor of Cytokine Signaling 1 Protein); EC 2.6.1.1 (Aspartate Aminotransferases); EC 2.7.10.2 (JAK1 protein, human); EC 2.7.10.2 (Janus Kinase 1); EC 2.7.10.2 (TYK2 Kinase); EC 2.7.10.2 (TYK2 protein, human); EC 2.7.7.- (OAS1 protein, human); EC 2.7.7.84 (2',5'-Oligoadenylate Synthetase); EC 3.1.- (Endoribonucleases); EC 3.1.26.- (2-5A-dependent ribonuclease)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170714
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180927


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[PMID]:28640813
[Au] Autor:Li H; Reksten TR; Ice JA; Kelly JA; Adrianto I; Rasmussen A; Wang S; He B; Grundahl KM; Glenn SB; Miceli-Richard C; Bowman S; Lester S; Eriksson P; Eloranta ML; Brun JG; Gøransson LG; Harboe E; Guthridge JM; Kaufman KM; Kvarnström M; Cunninghame Graham DS; Patel K; Adler AJ; Farris AD; Brennan MT; Chodosh J; Gopalakrishnan R; Weisman MH; Venuturupalli S; Wallace DJ; Hefner KS; Houston GD; Huang AJW; Hughes PJ; Lewis DM; Radfar L; Vista ES; Edgar CE; Rohrer MD; Stone DU; Vyse TJ; Harley JB; Gaffney PM; James JA; Turner S; Alevizos I; Anaya JM; Rhodus NL; Segal BM; for UK Primary Sjögren's Syndrome Registry
[Ad] Endereço:Arthritis and Clinical Immunology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, United States of America.
[Ti] Título:Identification of a Sjögren's syndrome susceptibility locus at OAS1 that influences isoform switching, protein expression, and responsiveness to type I interferons.
[So] Source:PLoS Genet;13(6):e1006820, 2017 Jun.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sjögren's syndrome (SS) is a common, autoimmune exocrinopathy distinguished by keratoconjunctivitis sicca and xerostomia. Patients frequently develop serious complications including lymphoma, pulmonary dysfunction, neuropathy, vasculitis, and debilitating fatigue. Dysregulation of type I interferon (IFN) pathway is a prominent feature of SS and is correlated with increased autoantibody titers and disease severity. To identify genetic determinants of IFN pathway dysregulation in SS, we performed cis-expression quantitative trait locus (eQTL) analyses focusing on differentially expressed type I IFN-inducible transcripts identified through a transcriptome profiling study. Multiple cis-eQTLs were associated with transcript levels of 2'-5'-oligoadenylate synthetase 1 (OAS1) peaking at rs10774671 (PeQTL = 6.05 × 10-14). Association of rs10774671 with SS susceptibility was identified and confirmed through meta-analysis of two independent cohorts (Pmeta = 2.59 × 10-9; odds ratio = 0.75; 95% confidence interval = 0.66-0.86). The risk allele of rs10774671 shifts splicing of OAS1 from production of the p46 isoform to multiple alternative transcripts, including p42, p48, and p44. We found that the isoforms were differentially expressed within each genotype in controls and patients with and without autoantibodies. Furthermore, our results showed that the three alternatively spliced isoforms lacked translational response to type I IFN stimulation. The p48 and p44 isoforms also had impaired protein expression governed by the 3' end of the transcripts. The SS risk allele of rs10774671 has been shown by others to be associated with reduced OAS1 enzymatic activity and ability to clear viral infections, as well as reduced responsiveness to IFN treatment. Our results establish OAS1 as a risk locus for SS and support a potential role for defective viral clearance due to altered IFN response as a genetic pathophysiological basis of this complex autoimmune disease.
[Mh] Termos MeSH primário: 2´,5´-Oligoadenilato Sintetase/genética
Interferon Tipo I/genética
Locos de Características Quantitativas/genética
Síndrome de Sjogren/genética
[Mh] Termos MeSH secundário: 2',5'-Oligoadenilato Sintetase/biossíntese
Alelos
Processamento Alternativo/genética
Feminino
Regulação da Expressão Gênica
Estudos de Associação Genética
Predisposição Genética para Doença
Seres Humanos
Interferon Tipo I/metabolismo
Masculino
Síndrome de Sjogren/metabolismo
Síndrome de Sjogren/patologia
Viroses/genética
Viroses/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interferon Type I); EC 2.7.7.- (OAS1 protein, human); EC 2.7.7.84 (2',5'-Oligoadenylate Synthetase)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171028
[Lr] Data última revisão:
171028
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1006820


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[PMID]:28444539
[Au] Autor:Tan Y; Yang T; Liu P; Chen L; Tian Q; Guo Y; He H; Liu Y; Chen Z
[Ad] Endereço:Department of Pediatrics, The Affiliated Hospital of Qingdao University, No. 59, Haier Road, Qingdao, 266000, China.
[Ti] Título:Association of the OAS3 rs1859330 G/A genetic polymorphism with severity of enterovirus-71 infection in Chinese Han children.
[So] Source:Arch Virol;162(8):2305-2313, 2017 Aug.
[Is] ISSN:1432-8798
[Cp] País de publicação:Austria
[La] Idioma:eng
[Ab] Resumo:The 2'5'-oligoadenylate synthetase (OAS) is an interferon (IFN)-induced protein that plays an important role in the antiviral action of IFN, with OAS3 being one of the four OAS classes (OAS1, OAS2, OAS3, OASL). The effect of OAS on several infectious viral diseases has been reported; however, a study of the effect of OAS3 on enterovirus 71 (EV71) is lacking. The purpose of this study was to evaluate the association of the OAS3 rs1859330 G/A genetic polymorphism with susceptibility and severity of EV71 infection. We investigated 370 Chinese Han children with hand-foot-mouth disease (HFMD) (214 of which were mild cases while 156 were severe). An improved multiplex ligation detection reaction (iMLDR) technique was carried out to examine the genotype. The AA genotype distribution (p = 0.002) and A allele frequency (OR = 1.83, 95% CI 1.32-2.52, p < 0.001) of OAS3 rs1859330 in severe cases were significantly higher than in mild cases. When comparing the different genotypes in EV71-infected patients, there were statistical differences in relation to rash (p = 0.03), oral ulcers (p = 0.005), pathologic reflex (p = 0.003), WBC counts (p = 0.032), CRP (p = 0.024), BG concentrations (p = 0.029), ALT (p = 0.02), and EEG (p = 0.019). However, there were no differences in relation to age, gender, AST, CK-MB, CT/ MRI, as well as some symptoms and signs (e.g. duration of fever (days), headache, convulsions, consciousness disturbance, paralysis, sign of meningeal irritation). In the cerebrospinal fluid (CSF) of severe cases, there were no differences in the levels of white cells, protein, glucose, chloride, lymphocytes and monocytes between the different genotypes. The plasma levels of IFN-γ in EV71-infected patients were significantly higher than in the control group (p < 0.01). IFN-γ concentrations in severe cases were lower in A allele carriers (AA+GA) (118.5 ± 12.6pg/mL) than in GG homozygotes (152.6 ± 56.3pg/mL p < 0.05). These findings suggest that the OAS3 rs1859330 G/A genetic polymorphism is associated with the severity of EV-71 infection, and that the A allele is a risk factor for the development of severe EV71 infection.
[Mh] Termos MeSH primário: 2´,5´-Oligoadenilato Sintetase/genética
Grupo com Ancestrais do Continente Asiático/genética
Doença de Mão, Pé e Boca/genética
Interferon gama/sangue
[Mh] Termos MeSH secundário: Criança
Pré-Escolar
China
Enterovirus Humano A
Feminino
Frequência do Gene
Predisposição Genética para Doença
Seres Humanos
Masculino
Polimorfismo de Nucleotídeo Único
Carga Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IFNG protein, human); 82115-62-6 (Interferon-gamma); EC 2.7.7.84 (2',5'-Oligoadenylate Synthetase); EC 2.7.7.84 (OAS3 protein, human)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170802
[Lr] Data última revisão:
170802
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170427
[St] Status:MEDLINE
[do] DOI:10.1007/s00705-017-3381-6


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[PMID]:28361289
[Au] Autor:Boonarkart C; Suptawiwat O; Sakorn K; Puthavathana P; Auewarakul P
[Ad] Endereço:Department of Microbiology, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, 10700, Thailand.
[Ti] Título:Exposure to cold impairs interferon-induced antiviral defense.
[So] Source:Arch Virol;162(8):2231-2237, 2017 Aug.
[Is] ISSN:1432-8798
[Cp] País de publicação:Austria
[La] Idioma:eng
[Ab] Resumo:It is commonly believed that exposure to low temperature increases susceptibility to viral infection in the human respiratory tract, but a molecular mechanism supporting this belief has yet to be discovered. In this study, we investigated the effect of low temperature on viral infection and innate defense in cell lines from the human respiratory tract and found that interferon-induced antiviral responses were impaired at low temperatures. Cells maintained at 25°C and 33°C expressed lower levels of myxovirus resistance protein 1 (MxA) and 2'5'-oligoadenylate synthetase 1 (OAS1) mRNAs when compared to cells maintained at 37°C after infection by seasonal influenza viruses. Exogenous ß-interferon treatment reduced the viral replication at 37°C, but not at 25°C. Our results suggest that the impairment of interferon-induced antiviral responses by low temperature is one of several mechanisms that could explain an increase in host susceptibility to respiratory viruses after exposure to cold temperature.
[Mh] Termos MeSH primário: Antivirais/farmacologia
Temperatura Baixa/efeitos adversos
Vírus da Influenza A/patogenicidade
Interferon beta/farmacologia
Replicação Viral/efeitos dos fármacos
[Mh] Termos MeSH secundário: 2',5'-Oligoadenilato Sintetase/metabolismo
Células HEK293
Seres Humanos
Vírus da Influenza A/efeitos dos fármacos
Vírus da Influenza A/fisiologia
Influenza Humana/virologia
Proteínas de Resistência a Myxovirus/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (MX1 protein, human); 0 (Myxovirus Resistance Proteins); 77238-31-4 (Interferon-beta); EC 2.7.7.- (OAS1 protein, human); EC 2.7.7.84 (2',5'-Oligoadenylate Synthetase)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170802
[Lr] Data última revisão:
170802
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170401
[St] Status:MEDLINE
[do] DOI:10.1007/s00705-017-3334-0


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[PMID]:28331099
[Au] Autor:Li LF; Yu J; Zhang Y; Yang Q; Li Y; Zhang L; Wang J; Li S; Luo Y; Sun Y; Qiu HJ
[Ad] Endereço:State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin, China.
[Ti] Título:Interferon-Inducible Oligoadenylate Synthetase-Like Protein Acts as an Antiviral Effector against Classical Swine Fever Virus via the MDA5-Mediated Type I Interferon-Signaling Pathway.
[So] Source:J Virol;91(11), 2017 Jun 01.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Classical swine fever virus (CSFV) is the causative agent of classical swine fever (CSF), which poses a serious threat to the global pig industry. Interferons (IFNs) and IFN-stimulated genes (ISGs) play a key role in host antiviral defense. We have previously screened the porcine 2'-5'-oligoadenylate synthetase-like protein (pOASL) as a potential anti-CSFV ISG using a reporter CSFV. This study aimed to clarify the underlying antiviral mechanism of pOASL against CSFV. We confirmed that CSFV replication was significantly suppressed in lentivirus-delivered, pOASL-overexpressing PK-15 cells, whereas silencing the expression of endogenous pOASL by small interfering RNAs markedly enhanced CSFV growth. In addition, the transcriptional level of pOASL was upregulated both and upon CSFV infection. Interestingly, the anti-CSFV effects of pOASL are independent of the canonical RNase L pathway but depend on the activation of the type I IFN response. Glutathione -transferase pulldown and coimmunoprecipitation assays revealed that pOASL interacts with MDA5, a double-stranded RNA sensor, and further enhances MDA5-mediated type I IFN signaling. Moreover, we showed that pOASL exerts anti-CSFV effects in an MDA5-dependent manner. In conclusion, pOASL suppresses CSFV replication via the MDA5-mediated type I IFN-signaling pathway. The host innate immune response plays an important role in mounting the initial resistance to viral infection. Here, we identify the porcine 2'-5'-oligoadenylate synthetase-like protein (pOASL) as an interferon (IFN)-stimulated gene (ISG) against classical swine fever virus (CSFV). We demonstrate that the anti-CSFV effects of pOASL depend on the activation of type I IFN response. In addition, we show that pOASL, as an MDA5-interacting protein, is a coactivator of MDA5-mediated IFN induction to exert anti-CSFV actions. This work will be beneficial to the development of novel anti-CSFV strategies by targeting pOASL.
[Mh] Termos MeSH primário: 2´,5´-Oligoadenilato Sintetase/metabolismo
Vírus da Febre Suína Clássica/fisiologia
Interações Hospedeiro-Patógeno
Interferon Tipo I/metabolismo
Helicase IFIH1 Induzida por Interferon/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Peste Suína Clássica/imunologia
Peste Suína Clássica/virologia
Vírus da Febre Suína Clássica/crescimento & desenvolvimento
Endorribonucleases/genética
Endorribonucleases/metabolismo
Glutationa Transferase/metabolismo
Imunidade Inata
Imunoprecipitação
Interferon Tipo I/genética
Interferon Tipo I/imunologia
Helicase IFIH1 Induzida por Interferon/genética
Helicase IFIH1 Induzida por Interferon/imunologia
RNA Interferente Pequeno/genética
Transdução de Sinais
Suínos
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interferon Type I); 0 (RNA, Small Interfering); EC 2.5.1.18 (Glutathione Transferase); EC 2.7.7.84 (2',5'-Oligoadenylate Synthetase); EC 3.1.- (Endoribonucleases); EC 3.1.26.- (2-5A-dependent ribonuclease); EC 3.6.4.13 (Interferon-Induced Helicase, IFIH1)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170727
[Lr] Data última revisão:
170727
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170324
[St] Status:MEDLINE


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[PMID]:27988795
[Au] Autor:Mahony R; Gargan S; Roberts KL; Bourke N; Keating SE; Bowie AG; O'Farrelly C; Stevenson NJ
[Ad] Endereço:School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute (TBSI), Trinity College Dublin, Dublin, Ireland.
[Ti] Título:A novel anti-viral role for STAT3 in IFN-α signalling responses.
[So] Source:Cell Mol Life Sci;74(9):1755-1764, 2017 May.
[Is] ISSN:1420-9071
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The cytokine, Interferon (IFN)-α, induces a wide spectrum of anti-viral mediators, via the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway. STAT1 and STAT2 are well characterised to upregulate IFN-stimulated gene (ISG) expression; but even though STAT3 is also activated by IFN-α, its role in anti-viral ISG induction is unclear. Several viruses, including Hepatitis C and Mumps, reduce cellular STAT3 protein levels, via the promotion of ubiquitin-mediated proteasomal degradation. This viral immune evasion mechanism suggests an undiscovered anti-viral role for STAT3 in IFN-α signalling. To investigate STAT3's functional involvement in this Type I IFN pathway, we first analysed its effect upon the replication of two viruses, Influenza and Vaccinia. Viral plaque assays, using Wild Type (WT) and STAT3-/- Murine Embryonic Fibroblasts (MEFs), revealed that STAT3 is required for the inhibition of Influenza and Vaccinia replication. Furthermore, STAT3 shRNA knockdown also enhanced Influenza replication and hindered induction of several, well characterised, anti-viral ISGs: PKR, OAS2, MxB and ISG15; while STAT3 expression had no effect upon induction of a separate ISG group: Viperin, IFI27, CXCL10 and CCL5. These discoveries reveal, for the first time, an anti-viral role for STAT3 in the IFN-α pathway and characterise a requirement for STAT3 in the expression of specific ISGs. These findings also identify STAT3 as a therapeutic target against viral infection and highlight it as an essential pathway component for endogenous and therapeutic IFN-α responsiveness.
[Mh] Termos MeSH primário: Interferon-alfa/metabolismo
Fator de Transcrição STAT3/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: 2',5'-Oligoadenilato Sintetase/metabolismo
Animais
Linhagem Celular
Técnicas de Silenciamento de Genes
Seres Humanos
Vírus da Influenza A/fisiologia
Camundongos
Proteínas de Resistência a Myxovirus
Vírus Vaccinia/fisiologia
eIF-2 Quinase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interferon-alpha); 0 (Myxovirus Resistance Proteins); 0 (STAT3 Transcription Factor); EC 2.7.11.1 (eIF-2 Kinase); EC 2.7.7.- (2',5'-oligoadenylate synthetase 2, human); EC 2.7.7.84 (2',5'-Oligoadenylate Synthetase)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170915
[Lr] Data última revisão:
170915
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161219
[St] Status:MEDLINE
[do] DOI:10.1007/s00018-016-2435-3


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[PMID]:27744359
[Au] Autor:Ospina FE; Echeverri A; Zambrano D; Suso JP; Martínez-Blanco J; Cañas CA; Tobón GJ
[Ad] Endereço:Rheumatology Unit, Fundación Valle del Lili, ICESI University.
[Ti] Título:Distinguishing infections vs flares in patients with systemic lupus erythematosus.
[So] Source:Rheumatology (Oxford);56(suppl_1):i46-i54, 2017 Apr 01.
[Is] ISSN:1462-0332
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:SLE is a chronic autoimmune disease involving multiple systems. Patients with SLE are highly susceptible to infections due to the combined effects of their immunosuppressive therapy and the abnormalities of the immune system that the disease itself causes, which can increase mortality in these patients. The differentiation of SLE activity and infection in a febrile patient with SLE is extremely difficult. Activity indexes are useful to identify patients with lupus flares but some clinical and biological abnormalities may, however, make it difficult to differentiate flares from infection. Several biological markers are now recognized as potential tools to establish the difference between SLE activity and infection, including CRP and procalcitonin. It is possible, however, that the use of only one biomarker is not sufficient to confirm or discard infection. This means that new scores, which include different biomarkers, might represent a better solution for differentiating these two clinical pictures. This review article describes several markers that are currently used, or have the potential, to differentiate infection from SLE flares.
[Mh] Termos MeSH primário: Infecção/diagnóstico
Lúpus Eritematoso Sistêmico/diagnóstico
[Mh] Termos MeSH secundário: 2',5'-Oligoadenilato Sintetase/metabolismo
Biomarcadores/metabolismo
Proteína C-Reativa/metabolismo
Calcitonina/metabolismo
Diagnóstico Diferencial
Progressão da Doença
Proteína HMGB1/metabolismo
Seres Humanos
Infecção/metabolismo
Contagem de Leucócitos
Lúpus Eritematoso Sistêmico/metabolismo
Lúpus Eritematoso Sistêmico/fisiopatologia
Lectina de Ligação a Manose/metabolismo
Glicoproteínas de Membrana/metabolismo
Neutrófilos
Receptores de IgG/metabolismo
Receptores Imunológicos/metabolismo
Receptor Gatilho 1 Expresso em Células Mieloides
Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers); 0 (HMGB1 Protein); 0 (HMGB1 protein, human); 0 (Mannose-Binding Lectin); 0 (Membrane Glycoproteins); 0 (Receptors, IgG); 0 (Receptors, Immunologic); 0 (TREM1 protein, human); 0 (Triggering Receptor Expressed on Myeloid Cells-1); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 7); 9007-12-9 (Calcitonin); 9007-41-4 (C-Reactive Protein); EC 2.7.7.84 (2',5'-Oligoadenylate Synthetase)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161017
[St] Status:MEDLINE
[do] DOI:10.1093/rheumatology/kew340



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