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[PMID]:29396713
[Au] Autor:Kiladjian JJ; Guglielmelli P; Griesshammer M; Saydam G; Masszi T; Durrant S; Passamonti F; Jones M; Zhen H; Li J; Gadbaw B; Perez Ronco J; Khan M; Verstovsek S
[Ad] Endereço:Centre d'Investigations Cliniques (CIC1427), Hôpital Saint-Louis, AP-HP, INSERM, CLIP2 "Saint-Louis - Paris Nord," Early Phase Research Center, Université Paris Diderot, 1, Avenue Claude Vellefaux, 75010, Paris, France. jean-jacques.kiladjian@aphp.fr.
[Ti] Título:Efficacy and safety of ruxolitinib after and versus interferon use in the RESPONSE studies.
[So] Source:Ann Hematol;97(4):617-627, 2018 Apr.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Ruxolitinib was well tolerated and superior to best available therapy (including interferon [IFN]) in controlling hematocrit without phlebotomy eligibility, normalizing blood counts, and improving polycythemia vera-related symptoms in the Study of Efficacy and Safety in Polycythemia Vera Subjects Who Are Resistant to or Intolerant of Hydroxyurea: JAK Inhibitor INC424 (INCB018424) Tablets Versus Best Available Care (RESPONSE) studies. This ad hoc analysis focuses on ruxolitinib in relation to IFN in the RESPONSE studies, with attention on the following: (1) safety and efficacy of ruxolitinib and best available therapy in patients who received IFN before study randomization, (2) safety and efficacy of IFN during randomized treatment in best available therapy arm, and (3) use of ruxolitinib after crossover from best available therapy in IFN-treated patients. IFN exposure before randomization had little effect on the efficacy or safety of ruxolitinib. In the randomized treatment arms, ruxolitinib was superior to IFN in efficacy [hematocrit control (RESPONSE = 60% of ruxolitinib vs 23% of IFN patients; RESPONSE-2 = 62% of ruxolitinib vs 15% of IFN patients)] and was tolerated better in hydroxyurea-resistant or hydroxyurea-intolerant patients. After crossing over to receive ruxolitinib, patients who had initially received IFN and did not respond had improved hematologic and spleen responses (62% of patients at any time after crossover) and an overall reduction in phlebotomy procedures. Rates and incidences of the most common adverse events decreased after crossover to ruxolitinib, except for infections (primarily grade 1 or 2). These data suggest that ruxolitinib is efficacious and well tolerated in patients who were previously treated with IFN. The RESPONSE (NCT01243944) and RESPONSE-2 (NCT02038036) studies were registered at clinicaltrials.gov .
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Interferons/uso terapêutico
Janus Quinases/antagonistas & inibidores
Policitemia Vera/tratamento farmacológico
Inibidores de Proteínas Quinases/uso terapêutico
Pirazóis/uso terapêutico
[Mh] Termos MeSH secundário: Adulto
Idoso
Antineoplásicos/efeitos adversos
Sangria/efeitos adversos
Terapia Combinada/efeitos adversos
Estudos Cross-Over
Monitoramento de Medicamentos
Resistência a Múltiplos Medicamentos
Resistência a Medicamentos Antineoplásicos
Feminino
Seres Humanos
Hidroxiureia/efeitos adversos
Hidroxiureia/uso terapêutico
Interferons/efeitos adversos
Janus Quinases/metabolismo
Masculino
Meia-Idade
Policitemia Vera/metabolismo
Policitemia Vera/fisiopatologia
Policitemia Vera/terapia
Padrões de Prática Médica
Inibidores de Proteínas Quinases/efeitos adversos
Pirazóis/efeitos adversos
Reprodutibilidade dos Testes
Esplenomegalia/etiologia
Esplenomegalia/prevenção & controle
[Pt] Tipo de publicação:CLINICAL TRIAL; CLINICAL TRIAL, PHASE III; COMPARATIVE STUDY; EQUIVALENCE TRIAL; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (INCB018424); 0 (Protein Kinase Inhibitors); 0 (Pyrazoles); 9008-11-1 (Interferons); EC 2.7.10.2 (Janus Kinases); X6Q56QN5QC (Hydroxyurea)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180204
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-017-3225-1


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[PMID]:28456632
[Au] Autor:Laidlaw SM; Marukian S; Gilmore RH; Cashman SB; Nechyporuk-Zloy V; Rice CM; Dustin LB
[Ad] Endereço:Kennedy Institute of Rheumatology, The University of Oxford, Oxford, United Kingdom; Peter Medawar Building for Pathogen Research, The University of Oxford, Oxford, United Kingdom.
[Ti] Título:Tumor Necrosis Factor Inhibits Spread of Hepatitis C Virus Among Liver Cells, Independent From Interferons.
[So] Source:Gastroenterology;153(2):566-578.e5, 2017 Aug.
[Is] ISSN:1528-0012
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND & AIMS: Tumor necrosis factor (TNF) is an inflammatory cytokine expressed by human fetal liver cells (HFLCs) after infection with cell culture-derived hepatitis C virus (HCV). TNF has been reported to increase entry of HCV pseudoparticles into hepatoma cells and inhibit signaling by interferon alpha (IFNα), but have no effect on HCV-RNA replication. We investigated the effects of TNF on HCV infection of and spread among Huh-7 hepatoma cells and primary HFLCs. METHODS: Human hepatoma (Huh-7 and Huh-7.5) and primary HFLCs were incubated with TNF and/or recombinant IFNA2A, IFNB, IFNL1, and IFNL2 before or during HCV infection. We used 2 fully infectious HCV chimeric viruses of genotype 2A in these studies: J6/JFH (clone 2) and Jc1(p7-nsGluc2A) (Jc1G), which encodes a secreted luciferase reporter. We measured HCV replication, entry, spread, production, and release in hepatoma cells and HFLCs. RESULTS: TNF inhibited completion of the HCV infectious cycle in hepatoma cells and HFLCs in a dose-dependent and time-dependent manner. This inhibition required TNF binding to its receptor. Inhibition was independent of IFNα, IFNß, IFNL1, IFNL2, or Janus kinase signaling via signal transducer and activator of transcription. TNF reduced production of infectious viral particles by Huh-7 and HFLC, and thereby reduced the number of infected cells and focus size. TNF had little effect on HCV replicons and increased entry of HCV pseudoparticles. When cells were incubated with TNF before infection, the subsequent antiviral effects of IFNs were increased. CONCLUSIONS: In a cell culture system, we found TNF to have antiviral effects independently of, as well as in combination with, IFNs. TNF inhibits HCV infection despite increased HCV envelope glycoprotein-mediated infection of liver cells. These findings contradict those from other studies, which have reported that TNF blocks signal transduction in response to IFNs. The destructive inflammatory effects of TNF must be considered along with its antiviral effects.
[Mh] Termos MeSH primário: Antivirais/farmacologia
Hepacivirus/efeitos dos fármacos
Hepatite C/tratamento farmacológico
Interferons/farmacologia
Fator de Necrose Tumoral alfa/farmacologia
[Mh] Termos MeSH secundário: Carcinoma Hepatocelular/virologia
Linhagem Celular Tumoral
Genótipo
Hepacivirus/genética
Hepatócitos/efeitos dos fármacos
Hepatócitos/virologia
Seres Humanos
Janus Quinases/metabolismo
Fígado/citologia
Neoplasias Hepáticas/virologia
Receptores do Fator de Necrose Tumoral/metabolismo
Replicon/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
Fator de Necrose Tumoral alfa/metabolismo
Replicação Viral/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (Receptors, Tumor Necrosis Factor); 0 (Tumor Necrosis Factor-alpha); 9008-11-1 (Interferons); EC 2.7.10.2 (Janus Kinases)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


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[PMID]:28747383
[Au] Autor:McDonough A; Lee RV; Noor S; Lee C; Le T; Iorga M; Phillips JLH; Murphy S; Möller T; Weinstein JR
[Ad] Endereço:Department of Neurology and.
[Ti] Título:Ischemia/Reperfusion Induces Interferon-Stimulated Gene Expression in Microglia.
[So] Source:J Neurosci;37(34):8292-8308, 2017 Aug 23.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Innate immune signaling is important in the pathophysiology of ischemia/reperfusion (stroke)-induced injury and recovery. Several lines of evidence support a central role for microglia in these processes. Recent work has identified Toll-like receptors (TLRs) and type I interferon (IFN) signaling in both ischemia/reperfusion-induced brain injury and ischemic preconditioning-mediated neuroprotection. To determine the effects of "ischemia/reperfusion-like" conditions on microglia, we performed genomic analyses on wild-type (WT) and cultured microglia after sequential exposure to hypoxia/hypoglycemia and normoxia/normoglycemia (H/H-N/N). We observed increased expression of type 1 IFN-stimulated genes (ISGs) as the predominant transcriptomal feature of H/H-N/N-exposed WT, but not , microglia. Microarray analysis on sorted microglia from ipsilateral male mouse cortex after a transient ischemic pulse also demonstrated robust expression of ISGs. Type 1 IFNs, including the IFN-αs and IFN-ß, activate the interferon-α/ß receptor (IFNAR) complex. We confirmed both H/H-N/N- and ischemia/reperfusion-induced microglial ISG responses by quantitative real-time PCR and demonstrated that both were dependent on IFNAR1. We characterized the effects of hypoxia/hypoglycemia on phosphorylation of signal transducer and activator of transcription 1 (STAT1), release of type 1 IFNs, and surface expression of IFNAR1 in microglia. We demonstrated that IFN-ß induces dose-dependent secretion of ISG chemokines in cultured microglia and robust ISG expression in microglia both and Finally, we demonstrated that the microglial ISG chemokine responses to TLR4 agonists were dependent on TLR4 and IFNAR1. Together, these data suggest novel ischemia/reperfusion-induced pathways for both TLR4-dependent and -independent, IFNAR1-dependent, type 1 IFN signaling in microglia. Stroke is the fifth leading cause of death in the United States and is a leading cause of serious long-term disability worldwide. Innate immune responses are critical in stroke pathophysiology, and microglia are key cellular effectors in the CNS response to ischemia/reperfusion. Using a transcriptional analysis approach, we identified a robust interferon (IFN)-stimulated gene response within microglia exposed to ischemia/reperfusion in both and experimental paradigms. Using a number of complementary techniques, we have demonstrated that these responses are dependent on innate immune signaling components including Toll-like receptor-4 and type I IFNs. We have also elucidated several novel ischemia/reperfusion-induced microglial signaling mechanisms.
[Mh] Termos MeSH primário: Isquemia Encefálica/metabolismo
Interferons/farmacologia
Microglia/metabolismo
Receptor de Interferon alfa e beta/biossíntese
Traumatismo por Reperfusão/metabolismo
Receptor 4 Toll-Like/deficiência
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Isquemia Encefálica/genética
Células Cultivadas
Relação Dose-Resposta a Droga
Feminino
Expressão Gênica
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Microglia/efeitos dos fármacos
Receptor de Interferon alfa e beta/genética
Traumatismo por Reperfusão/genética
Receptor 4 Toll-Like/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ifnar1 protein, mouse); 0 (Tlr4 protein, mouse); 0 (Toll-Like Receptor 4); 156986-95-7 (Receptor, Interferon alpha-beta); 9008-11-1 (Interferons)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180303
[Lr] Data última revisão:
180303
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.0725-17.2017


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[PMID]:29253356
[Au] Autor:Zhi X; Lv J; Wei Y; Du P; Chang Y; Zhang Y; Gao Y; Wu R
[Ad] Endereço:a College of Veterinary Medicine, Gansu Agricultural University, Lanzhou, 730070 Gansu, People's Republic of China.
[Ti] Título:Foot-and-mouth disease virus infection stimulates innate immune signaling in the mouse macrophage RAW 264.7 cells.
[So] Source:Can J Microbiol;64(2):155-166, 2018 Feb.
[Is] ISSN:1480-3275
[Cp] País de publicação:Canada
[La] Idioma:eng
[Ab] Resumo:The innate immune system acts as the first line of defense against invasion by bacterial and viral pathogens. The role of macrophages in innate immune responses to foot-and-mouth disease virus (FMDV) is poorly understood. To determine the mechanism underlying activation of innate immunity after FMDV infection in macrophages, we performed FMDV infection in mouse macrophage RAW 264.7 cells and found that FMDV serotype O infection induced a cytopathic effect. We then evaluated the gene expression profile in macrophage RAW 264.7 cells after FMDV infection using systematic microarray analysis. Gene ontology annotation and enrichment analysis revealed that FMDV promoted expression in a group of genes that are enriched in innate immune response and inflammatory response processes. Further research demonstrated that FMDV serotype O infection enhanced NF-κB, Toll-like, and RIG-I-like receptor signaling pathways and proteins expression and increased transcription and expression of a series of cytokines and interferons, as proved by qRT-PCR, Western blot, ELISA, and dual-luciferase reporter assay. Our study concluded that FMDV infection triggers the innate immune response in macrophages after activation of multiple innate immune pathway receptors and proteins by FMDV serotype O, resulting in activation and secretion of a series of cytokines and interferons.
[Mh] Termos MeSH primário: Vírus da Febre Aftosa/imunologia
Febre Aftosa/imunologia
Macrófagos/imunologia
Transdução de Sinais/imunologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Citocinas/genética
Citocinas/imunologia
Regulação da Expressão Gênica/imunologia
Imunidade Inata/genética
Interferons/genética
Interferons/imunologia
Camundongos
Células RAW 264.7
Transdução de Sinais/genética
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 9008-11-1 (Interferons)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE
[do] DOI:10.1139/cjm-2017-0348


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[PMID]:29253566
[Au] Autor:Hoshikawa M; Aoki T; Matsushita H; Karasaki T; Hosoi A; Odaira K; Fujieda N; Kobayashi Y; Kambara K; Ohara O; Arita J; Hasegawa K; Kakimi K; Kokudo N
[Ad] Endereço:Hepato-Biliary-Pancreatic Surgery Division, Department of Surgery, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo 113-8655, Japan.
[Ti] Título:NK cell and IFN signatures are positive prognostic biomarkers for resectable pancreatic cancer.
[So] Source:Biochem Biophys Res Commun;495(2):2058-2065, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:To establish prognostic biomarkers and to identify potential novel therapeutic targets, we performed integrative immunomonitoring of blood and tumor in patients with resectable pancreatic cancer. Flow cytometry (FC) was employed for phenotyping immune cells, multiplex bead assays for plasma cytokine and chemokine determination, and RNA-Seq for the analysis of gene expression in the tumor. Nineteen pancreatic cancer patients were stratified into those with longer or shorter than median recurrence-free survival after surgery (median, 426 days). There were no significant differences between the two groups for clinical parameters including age, sex, surgical procedure, stage, or postoperative adjuvant therapy. However, we found that the percentages of NK cells as assessed by FC in peripheral blood mononuclear cells were higher in patients with late recurrence (P = .037). RNA-Seq data indicated no differences in the amount of immune cells or stromal cells between the two groups, although NK cells in the tumor did tend to be higher in patients with late recurrence (P = .058). Type I and II IFN signatures were enriched in late-recurring tumors (FDR q-value <0.001), while genes related to KRAS signaling and the epithelial mesenchymal transition (EMT) were enriched in early recurrence. We conclude that tumor-intrinsic properties of metastasis and recurrence influence prognosis, whereas NK cells that might contribute to prevent metastasis are associated with longer recurrence-free survival. Therefore, enhancement of NK cell activity and inhibition of the EMT and KRAS signaling might represent appropriate therapeutic targets following surgical resection of pancreatic cancer.
[Mh] Termos MeSH primário: Interferons/metabolismo
Células Matadoras Naturais/patologia
Recidiva Local de Neoplasia/epidemiologia
Recidiva Local de Neoplasia/patologia
Neoplasias Pancreáticas/epidemiologia
Neoplasias Pancreáticas/patologia
[Mh] Termos MeSH secundário: Adulto
Distribuição por Idade
Idoso
Idoso de 80 Anos ou mais
Biomarcadores Tumorais
Intervalo Livre de Doença
Transição Epitelial-Mesenquimal
Feminino
Seres Humanos
Japão/epidemiologia
Masculino
Meia-Idade
Recidiva Local de Neoplasia/prevenção & controle
Neoplasias Pancreáticas/cirurgia
Prevalência
Prognóstico
Medição de Risco
Distribuição por Sexo
Taxa de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 9008-11-1 (Interferons)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE


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[PMID]:27771387
[Au] Autor:Alfaiate D; Lucifora J; Abeywickrama-Samarakoon N; Michelet M; Testoni B; Cortay JC; Sureau C; Zoulim F; Dény P; Durantel D
[Ad] Endereço:INSERM U1052, CNRS UMR-5286, Cancer Research Center of Lyon (CRCL), 69008 Lyon, France; University of Lyon, Université Claude-Bernard (UCBL), 69008 Lyon, France.
[Ti] Título:HDV RNA replication is associated with HBV repression and interferon-stimulated genes induction in super-infected hepatocytes.
[So] Source:Antiviral Res;136:19-31, 2016 12.
[Is] ISSN:1872-9096
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Hepatitis D virus (HDV) super-infection of Hepatitis B virus (HBV)-infected patients is the most aggressive form of viral hepatitis. HDV infection is not susceptible to direct anti-HBV drugs, and only suboptimal antiviral responses are obtained with interferon (IFN)-alpha-based therapy. To get insights on HDV replication and interplay with HBV in physiologically relevant hepatocytes, differentiated HepaRG (dHepaRG) cells, previously infected or not with HBV, were infected with HDV, and viral markers were extensively analyzed. Innate and IFN responses to HDV were monitored by measuring pro-inflammatory and interferon-stimulated gene (ISG) expression. Both mono- and super-infected dHepaRG cells supported a strong HDV intracellular replication, which was accompanied by a strong secretion of infectious HDV virions only in the super-infection setting and despite the low number of co-infected cells. Upon HDV super-infection, HBV replication markers including HBeAg, total HBV-DNA and pregenomic RNA were significantly decreased, confirming the interference of HDV on HBV. Yet, no decrease of circular covalently closed HBV DNA (cccDNA) and HBsAg levels was evidenced. At the peak of HDV-RNA accumulation and onset of interference on HBV replication, a strong type-I IFN response was observed, with interferon stimulated genes, RSAD2 (Viperin) and IFI78 (MxA) being highly induced. We established a cellular model to characterize in more detail the direct interference of HBV and HDV, and the indirect interplay between the two viruses via innate immune responses. This model will be instrumental to assess molecular and immunological mechanisms of this viral interference.
[Mh] Termos MeSH primário: Vírus da Hepatite B/fisiologia
Vírus Delta da Hepatite/fisiologia
Hepatócitos/virologia
Imunidade Inata
Interferons/imunologia
Interferência Viral
Replicação Viral
[Mh] Termos MeSH secundário: Células Cultivadas
Coinfecção
Replicação do DNA
DNA Circular
Hepatite B/virologia
Antígenos E da Hepatite B/genética
Hepatite D/virologia
Vírus Delta da Hepatite/genética
Seres Humanos
Interferon Tipo I/imunologia
Proteínas de Resistência a Myxovirus/genética
Proteínas/genética
RNA Viral/biossíntese
RNA Viral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA, Circular); 0 (Hepatitis B e Antigens); 0 (Interferon Type I); 0 (MX1 protein, human); 0 (Myxovirus Resistance Proteins); 0 (Proteins); 0 (RNA, Viral); 0 (RSAD2 protein, human); 9008-11-1 (Interferons)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161107
[St] Status:MEDLINE


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[PMID]:29180486
[Au] Autor:De La Cruz-Rivera PC; Kanchwala M; Liang H; Kumar A; Wang LF; Xing C; Schoggins JW
[Ad] Endereço:Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX 75390.
[Ti] Título:The IFN Response in Bats Displays Distinctive IFN-Stimulated Gene Expression Kinetics with Atypical RNASEL Induction.
[So] Source:J Immunol;200(1):209-217, 2018 01 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bats host a large number of zoonotic viruses, including several viruses that are highly pathogenic to other mammals. The mechanisms underlying this rich viral diversity are unknown, but they may be linked to unique immunological features that allow bats to act as asymptomatic viral reservoirs. Vertebrates respond to viral infection by inducing IFNs, which trigger antiviral defenses through IFN-stimulated gene (ISG) expression. Although the IFN system of several bats is characterized at the genomic level, less is known about bat IFN-mediated transcriptional responses. In this article, we show that IFN signaling in bat cells from the black flying fox ( ) consists of conserved and unique ISG expression profiles. In IFN-stimulated cells, bat ISGs comprise two unique temporal subclusters with similar early induction kinetics but distinct late-phase declines. In contrast, human ISGs lack this decline phase and remained elevated for longer periods. Notably, in unstimulated cells, bat ISGs were expressed more highly than their human counterparts. We also found that the antiviral effector 2-5A-dependent endoribonuclease, which is not an ISG in humans, is highly IFN inducible in black flying fox cells and contributes to cell-intrinsic control of viral infection. These studies reveal distinctive innate immune features that may underlie a unique virus-host relationship in bats.
[Mh] Termos MeSH primário: Antivirais/metabolismo
Quirópteros/imunologia
Endorribonucleases/metabolismo
Fatores Reguladores de Interferon/metabolismo
Viroses/imunologia
[Mh] Termos MeSH secundário: Animais
Doenças Assintomáticas
Linhagem Celular
Reservatórios de Doenças
Endorribonucleases/genética
Regulação da Expressão Gênica
Interações Hospedeiro-Patógeno
Seres Humanos
Imunidade Inata
Fatores Reguladores de Interferon/genética
Interferons/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (Interferon Regulatory Factors); 9008-11-1 (Interferons); EC 3.1.- (Endoribonucleases); EC 3.1.26.- (2-5A-dependent ribonuclease)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180131
[Lr] Data última revisão:
180131
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1701214


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[PMID]:29232714
[Au] Autor:Lee H; Park KH; Ryu JH; Choi AR; Yu JH; Lim J; Han K; Kim SI; Yang CW; Chung BH; Oh EJ
[Ad] Endereço:Department of Laboratory Medicine, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea.
[Ti] Título:Cytomegalovirus (CMV) immune monitoring with ELISPOT and QuantiFERON-CMV assay in seropositive kidney transplant recipients.
[So] Source:PLoS One;12(12):e0189488, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Although cytomegalovirus (CMV) specific cell-mediated immunity (CMI) has been suggested as a predictive marker for CMV infection, proper CMI monitoring strategy in CMV-seropositive recipients and optimal method are not defined. The aim of this study was to evaluate two interferon gamma release assays during early post-transplant period as a predictor of the development of CMV infection in CMV-seropositive patients. A total of 124 CMV-seropositive recipients who received kidney transplantation from CMV-seropositive donor were prospectively examined. At pre-transplant and post-transplant 1 and 3 months, CMV-CMIs were tested using QuantiFERON-CMV assay (QF-CMV) and CMV specific T cell ELISPOT against CMV pp65 and IE-1 antigens (pp65-ELISPOT, IE-1-ELISPOT). CMV DNAemia occurred in 16 (12.9%) patients within 3 months after transplant. Post-transplant pp65 or IE-1 ELISPOT response, but not QF-CMV, was significantly associated with CMV DNAemia. The pp65 ELISPOT (cut-off; 30 spots/200,000 cells) and IE-1 ELISPOT (10 spots/200,000 cells) at post-transplant 1 month predicted the risk of post-transplant CMV DNAemia (P = 0.019). Negative predictive values (NPV) for protection from CMV DNAemia in case of positive ELISPOT results were 94.5% (95% CI: 86.9-97.8%) and 97.6% (95% CI: 86.3-99.6%) in pp65-ELISPOT and IE-1-ELISPOT assays, respectively. These results suggest that the variability may exist between CMV ELISPOT assays and QF-CMV, and CMV ELISPOT at post-transplant 1 month can identify the risk of CMV DNAemia in seropositive kidney transplant recipients.
[Mh] Termos MeSH primário: Infecções por Citomegalovirus/diagnóstico
Ensaio de Imunoadsorção Enzimática/métodos
Interferons/sangue
Transplante de Rim
[Mh] Termos MeSH secundário: Adulto
Citomegalovirus/genética
Citomegalovirus/imunologia
Infecções por Citomegalovirus/imunologia
DNA Viral/sangue
Feminino
Seres Humanos
Imunossupressores/uso terapêutico
Interferons/imunologia
Masculino
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Viral); 0 (Immunosuppressive Agents); 9008-11-1 (Interferons)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171213
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189488


  9 / 20585 MEDLINE  
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[PMID]:29183527
[Au] Autor:Tanaka S; Tamori A; Takemura S; Hamano G; Ito T; Kawada N; Kubo S
[Ti] Título:Surgical Outcomes in Hepatitis C Virus-Related Hepatocellular Carcinoma: Special Reference to Sustained Virological Responses to Interferon Therapy.
[So] Source:Am Surg;83(11):1246-1255, 2017 Nov 01.
[Is] ISSN:1555-9823
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Long-term surgical outcomes after hepatic resection for hepatitis C virus (HCV)-related hepatocellular carcinoma (HCC) in patients who achieved a sustained virological response (SVR) to interferon (IFN) therapy remain inconclusive. Clinical records of 277 patients who underwent hepatic resection for HCV-related early stage HCC (met the Milan criteria) between 1993 and 2012 were retrospectively reviewed. Thirty-seven patients achieved the SVR during HCC detection (pre-SVR group), whereas 23 achieved SVR using adjuvant interferon therapy after hepatic resection (post-SVR group). The control group included remaining 217 patients. We investigated the SVR effects on surgical outcomes. Disease-free survival (DFS) rates at 5/10/15 years after hepatic resection were significantly greater in the pre and post-SVR groups than in the control group (46/30/30per cent and 61/36/27 per cent vs 23/7/7 per cent, respectively; P < 0.001). Overall survival (OS) rates at 10/15 years after hepatic resection were better in the pre- and post-SVR groups than in the control group (68/68 percent and 78/78 per cent vs 13/11 per cent, respectively; P < 0.001). On multivariate analysis, pre- and post-SVR were independent factors for no recurrence (pre-SVR: hazard ratio (HR), 0.48, P = 0.002; post-SVR: HR, 0.41, P = 0.001) and improved survival (pre-SVR: HR, 0.36, P = 0.002; post-SVR: HR, 0.122, P < 0.001). Achievement of SVR in patients with HCV-related HCC was associated with long-term disease-free survival and OS after hepatic resection.
[Mh] Termos MeSH primário: Antivirais/uso terapêutico
Carcinoma Hepatocelular/cirurgia
Hepatite C Crônica/tratamento farmacológico
Interferons/uso terapêutico
Neoplasias Hepáticas/cirurgia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Carcinoma Hepatocelular/mortalidade
Carcinoma Hepatocelular/virologia
Estudos de Casos e Controles
Intervalo Livre de Doença
Quimioterapia Combinada
Feminino
Hepatite C Crônica/mortalidade
Seres Humanos
Neoplasias Hepáticas/mortalidade
Neoplasias Hepáticas/virologia
Masculino
Meia-Idade
Recidiva Local de Neoplasia/mortalidade
Recidiva Local de Neoplasia/virologia
Estudos Retrospectivos
Ribavirina/uso terapêutico
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiviral Agents); 49717AWG6K (Ribavirin); 9008-11-1 (Interferons)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171204
[Lr] Data última revisão:
171204
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE


  10 / 20585 MEDLINE  
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[PMID]:29045448
[Au] Autor:Uemura H; Tsukada K; Mizushima D; Aoki T; Watanabe K; Kinai E; Teruya K; Gatanaga H; Kikuchi Y; Sugiyama M; Mizokami M; Oka S
[Ad] Endereço:AIDS Clinical Center, National Center for Global Health and Medicine, Tokyo, Japan.
[Ti] Título:Interferon-free therapy with direct acting antivirals for HCV/HIV-1 co-infected Japanese patients with inherited bleeding disorders.
[So] Source:PLoS One;12(10):e0186255, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Almost 30 years ago, about 30% of Japanese hemophiliacs became infected with HIV-1 and hepatitis C virus (HCV) after receiving contaminated blood products. While several studies have reported the high efficacy and safety of direct acting antivirals (DAA) in HIV-1 co-infected patients, such data are limited in hemophiliacs. METHODS: We conducted a single-center, open-label study involving 27 Japanese patients (median age; 45 years) with inherited bleeding disorders who were co-infected with HCV/HIV-1. Patients with HCV genotype 1 (GT1) and GT4 received ledipasvir (90 mg) plus sofosbuvir (400 mg), those with HCV GT2 received sofosbuvir plus weight-based ribavirin, and those with HCV GT3 received daclatasvir (60 mg) plus sofosbuvir. Treatment was continued for 12 weeks in all patients. The primary endpoints were rate of sustained virologic response at 12 weeks after end of therapy (SVR12) and occurrence of adverse events during DAA therapy. RESULTS: Eighteen (67%) patients had had received interferon-based therapy, and 11 (41%) had compensated cirrhosis. HCV genotypes were GT1a 4 (15%), GT1b 16 (59%), GT1 undetermined 2 (7%), GT2a 1 (4%), GT3a 3 (11%) and GT4a 1 (4%). All patients were on combination antiretroviral therapy (cART) and had undetectable HIV-1 viral load (<20 copies/µL) at baseline. All patients achieved SVR12. Serious adverse events were observed in 3 patients: arteritis of the leg, which resolved after completion of DAA therapy, asymptomatic QT prolongation and gastrointestinal hemorrhage. cART failure was noted in one patient due to emergence of raltegravir resistance during ledipasvir/sofosbuvir treatment. Although α-fetoprotein, Mac-2 binding protein glycosylation isomer (M2BPGi), and Fibro Scan (FS) scores decreased in most patients during DAA therapy, M2BPGi (>2.0 cutoff index) and FS scores (>15.0 kPa) were still high in 6 patients at week 36. CONCLUSIONS: DAA therapy is effective in all patients. However, adverse events and efficacy of cART should be monitored closely.
[Mh] Termos MeSH primário: Antivirais/administração & dosagem
Coinfecção/tratamento farmacológico
Infecções por HIV/tratamento farmacológico
Hemofilia A/tratamento farmacológico
Hepatite C Crônica/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Antivirais/efeitos adversos
Benzimidazóis/administração & dosagem
Coinfecção/complicações
Coinfecção/virologia
Quimioterapia Combinada/efeitos adversos
Feminino
Fluorenos/administração & dosagem
Infecções por HIV/complicações
Infecções por HIV/virologia
HIV-1/efeitos dos fármacos
HIV-1/patogenicidade
Hemofilia A/complicações
Hemofilia A/virologia
Hepacivirus/efeitos dos fármacos
Hepacivirus/patogenicidade
Hepatite C Crônica/complicações
Hepatite C Crônica/virologia
Seres Humanos
Imidazóis/administração & dosagem
Interferons/uso terapêutico
Cirrose Hepática/complicações
Cirrose Hepática/tratamento farmacológico
Cirrose Hepática/virologia
Masculino
Meia-Idade
RNA Viral/efeitos dos fármacos
Sofosbuvir/administração & dosagem
Carga Viral/efeitos dos fármacos
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (BMS-790052); 0 (Benzimidazoles); 0 (Fluorenes); 0 (Imidazoles); 0 (RNA, Viral); 013TE6E4WV (ledipasvir); 9008-11-1 (Interferons); WJ6CA3ZU8B (Sofosbuvir)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171019
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186255



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