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[PMID]:28789967
[Au] Autor:Zhang S; Cao X; Gao Q; Liu Y
[Ad] Endereço:Liver Cancer Institute, Zhongshan Hospital, Key Laboratory of Carcinogenesis and Cancer Invasion (Ministry of Education), Fudan University, Shanghai 200032, China.
[Ti] Título:Protein glycosylation in viral hepatitis-related HCC: Characterization of heterogeneity, biological roles, and clinical implications.
[So] Source:Cancer Lett;406:64-70, 2017 Oct 10.
[Is] ISSN:1872-7980
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Protein glycosylation is one of the most frequent and well-known posttranslational modifications, playing important roles in physiopathological processes. Glycosylation is catalyzed by enzymatic additions of heterogeneous glycans with specific linkage of monosaccharides and, in a preformed fashion, to specific amino acids within glycoproteins. Altered glycan macroheterogeneity and microheterogeneity have been reported in glycoproteins produced mainly by the liver, facilitating tumorigenesis, progression, and metastasis. Characterizing the heterogeneity and biological functions of glycans in liver diseases would lead to a better understanding of the molecular pathogenesis of liver damage and cancer, providing novel diagnostic, prognostic, and therapeutic clues. Technical advances in glycoproteomics and glycomics have allowed a more comprehensive and deeper understanding of disease-related glycosylation events. Here, we briefly review the structural diversity of glycans in viral hepatitis -related hepatocellular carcinoma, discuss their roles in regulating the initiation and development of liver cancer, and introduce potential clinical applications.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/patologia
Glicoproteínas/metabolismo
Vírus de Hepatite/fisiologia
Hepatite Viral Humana/complicações
Neoplasias Hepáticas/patologia
Polissacarídeos/metabolismo
[Mh] Termos MeSH secundário: Carcinoma Hepatocelular/metabolismo
Carcinoma Hepatocelular/virologia
Glicosilação
Seres Humanos
Neoplasias Hepáticas/metabolismo
Neoplasias Hepáticas/virologia
Polissacarídeos/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Glycoproteins); 0 (Polysaccharides)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170921
[Lr] Data última revisão:
170921
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE


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[PMID]:28669008
[Au] Autor:Zhou X; Lisenko K; Lehners N; Egerer G; Ho AD; Witzens-Harig M
[Ad] Endereço:Department of Hematology, Oncology and Rheumatology, Heidelberg University Hospital, University of Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany. zhou8285@126.com.
[Ti] Título:The influence of rituximab-containing chemotherapy on HCV load in patients with HCV-associated non-Hodgkin's lymphomas.
[So] Source:Ann Hematol;96(9):1501-1507, 2017 Sep.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Efficacy and safety of rituximab treatment in patients with Hepatitis C virus (HCV) infection associated non-Hodgkin's lymphoma (NHL) are still disputable. The aim of this study was to evaluate the influence of rituximab-containing chemotherapy on HCV load. Fifty-four patients with both HCV infection and NHL were identified between 2000 and 2016 at our institution. We retrospectively analyzed patients' demographic characteristics, treatment, and kinetics of HCV load before and after treatment with rituximab-containing chemotherapy. In the total group of 54 patients, 29 (54%) received rituximab. Both HCV load pre rituximab and maximal HCV load post rituximab were available in 16 patients. Overall, we observed no significant difference between HCV load pre rituximab and the maximal HCV load post rituximab (P = 0.19). In a patient who was treated simultaneously with direct-acting antivirals (DAAs) and rituximab-containing chemotherapy, HCV load decreased below the sensitivity level (≤12 IU/ml) during treatment. When regarding the influence of rituximab-containing chemotherapy alone on HCV load, we observed a significant elevation of HCV load (P = 0.04). Rituximab-containing chemotherapy may lead to an increase of HCV load in patients with HCV-associated NHL. However, this finding is based on small patient cohort and should be confirmed in larger clinical trials.
[Mh] Termos MeSH primário: Antivirais/administração & dosagem
Hepatite C
Vírus de Hepatite
Linfoma não Hodgkin
Rituximab/administração & dosagem
Carga Viral/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adulto
Idoso
Feminino
Hepatite C/sangue
Hepatite C/tratamento farmacológico
Seres Humanos
Linfoma não Hodgkin/sangue
Linfoma não Hodgkin/tratamento farmacológico
Masculino
Meia-Idade
Estudos Retrospectivos
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiviral Agents); 4F4X42SYQ6 (Rituximab)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170703
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-017-3058-y


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[PMID]:28502443
[Au] Autor:Karnsakul W; Schwarz KB
[Ad] Endereço:Pediatric Liver Center, Department of Pediatrics, Johns Hopkins University School of Medicine, 600 North Wolfe Street, CMSC 2-117, Baltimore, MD 21287, USA. Electronic address: wkarnsa1@jhmi.edu.
[Ti] Título:Hepatitis B and C.
[So] Source:Pediatr Clin North Am;64(3):641-658, 2017 Jun.
[Is] ISSN:1557-8240
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Chronic viral hepatitis is a global health threat and financial burden. Hepatitis B and C viruses (HBV and HCV) are the most common causes of chronic viral hepatitis in the United States. Most cases are asymptomatic before adulthood. Research has resulted in effective therapy for HCV and the promise of effective therapies for HBV. For HCV, therapy is pegylated interferon and ribavirin. Clinical trials with effective direct-acting antiviral agents are underway in pediatrics. For HBV, approved agents are alpha-interferon, lamivudine, adefovir, tenofovir, and entecavir. However, treatment seldom results in functional cure and more effective therapies are urgently needed.
[Mh] Termos MeSH primário: Antivirais/uso terapêutico
Hepatite B/tratamento farmacológico
Hepatite C/tratamento farmacológico
Vírus de Hepatite/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adolescente
Adulto
Criança
Pré-Escolar
Feminino
Hepatite B/diagnóstico
Hepatite C/diagnóstico
Seres Humanos
Masculino
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antiviral Agents)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170516
[St] Status:MEDLINE


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[PMID]:28426876
[Au] Autor:Kuramoto J; Arai E; Tian Y; Funahashi N; Hiramoto M; Nammo T; Nozaki Y; Takahashi Y; Ito N; Shibuya A; Ojima H; Sukeda A; Seki Y; Kasama K; Yasuda K; Kanai Y
[Ad] Endereço:Department of Pathology, Keio University School of Medicine, Tokyo 160-8582, Japan.
[Ti] Título:Genome-wide DNA methylation analysis during non-alcoholic steatohepatitis-related multistage hepatocarcinogenesis: comparison with hepatitis virus-related carcinogenesis.
[So] Source:Carcinogenesis;38(3):261-270, 2017 Mar 01.
[Is] ISSN:1460-2180
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to clarify the significance of DNA methylation alterations during non-alcoholic steatohepatitis (NASH)-related hepatocarcinogenesis. Single-CpG-resolution genome-wide DNA methylation analysis was performed on 264 liver tissue samples using the Illumina Infinium HumanMethylation450 BeadChip. After Bonferroni correction, 3331 probes showed significant DNA methylation alterations in 113 samples of non-cancerous liver tissue showing NASH (NASH-N) as compared with 55 samples of normal liver tissue (NLT). Principal component analysis using the 3331 probes revealed distinct DNA methylation profiles of NASH-N samples that were different from those of NLT samples and 37 samples of non-cancerous liver tissue showing chronic hepatitis or cirrhosis associated with hepatitis B virus (HBV) or hepatitis C virus (HCV) infection (viral-N). Receiver operating characteristic curve analysis identified 194 probes that were able to discriminate NASH-N samples from viral-N samples with area under the curve values of more than 0.95. Jonckheere-Terptsra trend test revealed that DNA methylation alterations in NASH-N samples from patients without hepatocellular carcinoma (HCC) were inherited by or strengthened in NASH-N samples from patients with HCC, and then inherited by or further strengthened in 22 samples of NASH-related HCC (NASH-T) themselves. NASH- and NASH-related HCC-specific DNA methylation alterations, which were not evident in viral-N samples and 37 samples of HCC associated with HBV or HCV infection, were observed in tumor-related genes, such as WHSC1, and were frequently associated with mRNA expression abnormalities. These data suggested that NASH-specific DNA methylation alterations may participate in NASH-related multistage hepatocarcinogenesis.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/genética
Metilação de DNA/genética
Neoplasias Hepáticas/genética
Hepatopatia Gordurosa não Alcoólica/genética
[Mh] Termos MeSH secundário: Adulto
Carcinogênese/genética
Carcinoma Hepatocelular/patologia
Carcinoma Hepatocelular/virologia
Linhagem Celular Tumoral
Ilhas de CpG/genética
Feminino
Vírus de Hepatite/patogenicidade
Seres Humanos
Fígado/metabolismo
Fígado/patologia
Fígado/virologia
Neoplasias Hepáticas/patologia
Neoplasias Hepáticas/virologia
Masculino
Meia-Idade
Hepatopatia Gordurosa não Alcoólica/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[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:170421
[St] Status:MEDLINE
[do] DOI:10.1093/carcin/bgx005


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[PMID]:28274850
[Au] Autor:Comarmond C; Garrido M; Pol S; Desbois AC; Costopoulos M; Le Garff-Tavernier M; Si Ahmed SN; Alric L; Fontaine H; Bellier B; Maciejewski A; Rosenzwajg M; Klatzmann D; Musset L; Poynard T; Cacoub P; Saadoun D
[Ad] Endereço:Département Hospitalo-Universitaire Inflammation-Immunopathologie-Biotherapie (département hospitalo-unniversitaire i2B), Sorbonne Universités, Université Pierre et Marie Curie Université Paris 06, unité mixte de recherche 7211, Paris, France; INSERM, unité mixte de recherche_S 959, Paris, France; c
[Ti] Título:Direct-Acting Antiviral Therapy Restores Immune Tolerance to Patients With Hepatitis C Virus-Induced Cryoglobulinemia Vasculitis.
[So] Source:Gastroenterology;152(8):2052-2062.e2, 2017 Jun.
[Is] ISSN:1528-0012
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND & AIMS: Interferon-free direct-acting antiviral (DAA) therapies are effective in patients with hepatitis C virus-induced cryoglobulinemia vasculitis (HCV-CV). We analyzed blood samples from patients with HCV-CV before and after DAA therapy to determine mechanisms of these drugs and their effects on cellular immunity. METHODS: We performed a prospective study of 27 consecutive patients with HCV-CV (median age, 59 y) treated with DAA therapy (21 patients received sofosbuvir plus ribavirin for 24 weeks, 4 patients received sofosbuvir plus daclatasvir for 12 weeks, and 2 patients received sofosbuvir plus simeprevir for 12 weeks) in Paris, France. Blood samples were collected from these patients before and after DAA therapy, and also from 12 healthy donors and 12 individuals with HCV infection without CV. HCV load, cryoglobulins, and cytokines were quantified by flow cytometry, cytokine multiplex assays, and enzyme-linked immunosorbent assay. RESULTS: Twenty-four patients (88.9%) had a complete clinical response of CV to DAA therapy at week 24, defined by improvement of all the affected organs and the absence of relapse. Compared with healthy donors and patients with HCV infection without CV, patients with HCV-CV, before DAA therapy, had a lower percentage of CD4+CD25hiFoxP3+ regulatory T cells (P < .01), but higher proportions of IgM+CD21-/low memory B cells (P < .05), CD4+IFNγ+ cells (P < .01), CD4+IL17A+ cells (P < .01), and CD4+CXCR5+interleukin 21+ follicular T-helper (Tfh) cells (P < .01). In patients with HCV-CV, there was a negative correlation between numbers of IgM+CD21-/low memory B cells and T-regulatory cells (P = .03), and positive correlations with numbers of Tfh cells (P = .03) and serum levels of cryoglobulin (P = .01). DAA therapy increased patients' numbers of T-regulatory cells (1.5% ± 0.18% before therapy vs 2.1% ± 0.18% after therapy), decreased percentages of IgM+CD21-/low memory B cells (35.7% ± 6.1% before therapy vs 14.9% ± 3.8% after therapy), and decreased numbers of Tfh cells (12% ± 1.3% before therapy vs 8% ± 0.9% after therapy). Expression levels of B lymphocyte stimulator receptor 3 and programmed cell death 1 on B cells increased in patients with HCV-CV after DAA-based therapy (mean fluorescence units, 37 ± 2.4 before therapy vs 47 ± 2.6 after therapy, P < .01; and 29 ± 7.3 before therapy vs 48 ± 9.3 after therapy, P < .05, respectively). CONCLUSIONS: In a prospective clinical trial of patients with HCV-CV, DAA-based therapy restored disturbances in peripheral B- and T-cell homeostasis.
[Mh] Termos MeSH primário: Antivirais/uso terapêutico
Subpopulações de Linfócitos B/efeitos dos fármacos
Crioglobulinemia/tratamento farmacológico
Hepatite C/tratamento farmacológico
Vírus de Hepatite/efeitos dos fármacos
Imidazóis/uso terapêutico
Tolerância Imunológica/efeitos dos fármacos
Imunidade Celular/efeitos dos fármacos
Ribavirina/uso terapêutico
Simeprevir/uso terapêutico
Sofosbuvir/uso terapêutico
Subpopulações de Linfócitos T/efeitos dos fármacos
Vasculite/tratamento farmacológico
[Mh] Termos MeSH secundário: Idoso
Antivirais/efeitos adversos
Subpopulações de Linfócitos B/imunologia
Subpopulações de Linfócitos B/metabolismo
Subpopulações de Linfócitos B/virologia
Biomarcadores/sangue
Estudos de Casos e Controles
Crioglobulinemia/diagnóstico
Crioglobulinemia/imunologia
Crioglobulinemia/virologia
Citocinas/sangue
Quimioterapia Combinada
Feminino
Hepatite C/complicações
Hepatite C/diagnóstico
Hepatite C/imunologia
Vírus de Hepatite/imunologia
Seres Humanos
Imidazóis/efeitos adversos
Masculino
Meia-Idade
Fenótipo
Estudos Prospectivos
Ribavirina/efeitos adversos
Simeprevir/efeitos adversos
Sofosbuvir/efeitos adversos
Subpopulações de Linfócitos T/imunologia
Subpopulações de Linfócitos T/metabolismo
Subpopulações de Linfócitos T/virologia
Fatores de Tempo
Resultado do Tratamento
Vasculite/diagnóstico
Vasculite/imunologia
Vasculite/virologia
Carga Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (BMS-790052); 0 (Biomarkers); 0 (Cytokines); 0 (Imidazoles); 49717AWG6K (Ribavirin); 9WS5RD66HZ (Simeprevir); WJ6CA3ZU8B (Sofosbuvir)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE


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[PMID]:27993129
[Au] Autor:Belyhun Y; Maier M; Mulu A; Diro E; Liebert UG
[Ad] Endereço:Institute of Virology, Faculty of Medicine, Leipzig University, Leipzig, Germany. belyhun@gmail.com.
[Ti] Título:Hepatitis viruses in Ethiopia: a systematic review and meta-analysis.
[So] Source:BMC Infect Dis;16(1):761, 2016 Dec 19.
[Is] ISSN:1471-2334
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The existing seroepidemiological data on viral hepatitis in Ethiopia showed a wide variation in prevalence pattern and the clinical and public health burden have been underestimated. The aim of this systematic review and meta-analysis was to provide a clear and comprehensive estimation of viral hepatitis epidemiology and the potential clinical burdens in Ethiopia. METHODS: A comprehensive literature search was carried out from five decades (1968-2015) published studies from biomedical databases; PubMed, Google scholar, Medline and Web of Science. RESULTS: The overall pooled prevalence of hepatitis B virus (HBV) was 7.4% (95%CI: 6.5-8.4). The pooled prevalence among subgroups showed 5.2% (95%CI: 3.7-7.4) in human immunodeficiency virus (HIV) infected individuals, 8.0% (95%CI: 5.9-10.7) in community based studies, 8.4% (95%CI: 5.4-12.7) in blood donors, 11.0% (95%CI: 7.5-15.9) in immigrants and 6.9% (95%CI: 5.6-8.5) in other groups. Among study parameters considered during meta-regression analysis, only study years were associated with a decreasing HBV prevalence rate over time. The overall pooled prevalence of anti-hepatitis C virus antibody (anti-HCV) was 3.1% (95%CI: 2.2-4.4). Unlike HBV, the anti-HCV prevalence in HIV infected individuals was higher (5.5%, 95%CI: 3.8-7.8%, p = 0.01) than the prevalence observed in the other subgroup of study population. Although relatively few data were available, hepatitis virus A (HAV), D (HDV) and E (HEV) were also circulated in Ethiopia. CONCLUSIONS: This review indicates that all types of viral hepatitis origins are endemic in Ethiopia. Adapting a recommended diagnostic and treatment algorithm of viral hepatitis in the routine healthcare systems and implementing prevention and control policies in the general population needs an urgent attention.
[Mh] Termos MeSH primário: Hepatite Viral Humana/epidemiologia
[Mh] Termos MeSH secundário: Infecções Oportunistas Relacionadas com a AIDS/epidemiologia
Adolescente
Adulto
Doadores de Sangue/estatística & dados numéricos
Coinfecção/epidemiologia
Etiópia/epidemiologia
Infecções por HIV/epidemiologia
Infecções por HIV/virologia
Hepatite B/epidemiologia
Hepatite B/virologia
Vírus da Hepatite B/imunologia
Vírus da Hepatite B/patogenicidade
Hepatite C/epidemiologia
Anticorpos Anti-Hepatite C/sangue
Vírus de Hepatite/patogenicidade
Hepatite Viral Humana/virologia
Seres Humanos
Meia-Idade
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (Hepatitis C Antibodies)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170619
[Lr] Data última revisão:
170619
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161221
[St] Status:MEDLINE


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[PMID]:27894309
[Au] Autor:Zhang Q; Matsuura K; Kleiner DE; Zamboni F; Alter HJ; Farci P
[Ad] Endereço:Laboratory of Infectious Diseases, Hepatic Pathogenesis Section, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD, 20892, USA.
[Ti] Título:Analysis of long noncoding RNA expression in hepatocellular carcinoma of different viral etiology.
[So] Source:J Transl Med;14(1):328, 2016 Nov 28.
[Is] ISSN:1479-5876
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Dysregulation of long noncoding RNA (lncRNA) expression contributes to the pathogenesis of many human diseases, including liver diseases. Several lncRNAs have been reported to play a role in the development of hepatocellular carcinoma (HCC). However, most studies have analyzed lncRNAs only in hepatitis B virus (HBV)-related HCC or in a single group of HCC patients regardless of the viral etiology. METHODS: To investigate whether lncRNAs are differentially expressed in HCC of different viral etiology, we profiled 101 disease-related lncRNAs, including 25 lncRNAs previously associated with HCC, in liver specimens obtained from well-characterized patients with HBV-, hepatitis C virus (HCV)-, or hepatitis D virus (HDV)-associated HCC. RESULTS: We identified eight novel HCC-related lncRNAs that were significantly dysregulated in HCC tissues compared to their surrounding non-tumorous tissues. Some of these lncRNAs were significantly dysregulated predominantly in one specific hepatitis virus-related HCC, including PCAT-29 in HBV-related HCC, aHIF and PAR5 in HCV-related HCC, and Y3 in HDV-related HCC. Among the lncRNAs previously reported in HCC, we found that DBH-AS1, hDREH and hPVT1 were differentially expressed in HCC of different viral etiology. CONCLUSIONS: Our study suggests that HCC of different viral etiology is regulated by different lncRNAs. The identification of lncRNAs unique to specific hepatitis virus-related HCC may provide new tools for improving the diagnosis of HCC and open new avenues for disease-specific therapeutic interventions.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/genética
Carcinoma Hepatocelular/virologia
Regulação Neoplásica da Expressão Gênica
Vírus de Hepatite/fisiologia
Neoplasias Hepáticas/genética
Neoplasias Hepáticas/virologia
RNA Longo não Codificante/genética
[Mh] Termos MeSH secundário: Carcinoma Hepatocelular/patologia
Perfilação da Expressão Gênica
Seres Humanos
Neoplasias Hepáticas/patologia
Análise de Componente Principal
RNA Longo não Codificante/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Long Noncoding)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161130
[St] Status:MEDLINE


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[PMID]:27834318
[Au] Autor:Satsangi S; Dhiman RK
[Ad] Endereço:Department of Hepatology, Postgraduate Institute of Medical Education & Research, Chandigarh 160 012, India.
[Ti] Título:Combating the wrath of viral hepatitis in India.
[So] Source:Indian J Med Res;144(1):1-5, 2016 Jul.
[Is] ISSN:0971-5916
[Cp] País de publicação:India
[La] Idioma:eng
[Mh] Termos MeSH primário: Vírus de Hepatite/patogenicidade
Hepatite Viral Humana/epidemiologia
[Mh] Termos MeSH secundário: Vírus de Hepatite/classificação
Hepatite Viral Humana/classificação
Hepatite Viral Humana/prevenção & controle
Hepatite Viral Humana/virologia
Seres Humanos
Índia
[Pt] Tipo de publicação:EDITORIAL
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161112
[St] Status:MEDLINE
[do] DOI:10.4103/0971-5916.193275


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[PMID]:27610716
[Au] Autor:Yugo DM; Hauck R; Shivaprasad HL; Meng XJ
[Ad] Endereço:A Department of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine, Virginia Polytechnic Institute and State University, 1981 Kraft Drive, Blacksburg, VA 24061-0913.
[Ti] Título:Hepatitis Virus Infections in Poultry.
[So] Source:Avian Dis;60(3):576-88, 2016 Sep.
[Is] ISSN:1938-4351
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Viral hepatitis in poultry is a complex disease syndrome caused by several viruses belonging to different families including avian hepatitis E virus (HEV), duck hepatitis B virus (DHBV), duck hepatitis A virus (DHAV-1, -2, -3), duck hepatitis virus Types 2 and 3, fowl adenoviruses (FAdV), and turkey hepatitis virus (THV). While these hepatitis viruses share the same target organ, the liver, they each possess unique clinical and biological features. In this article, we aim to review the common and unique features of major poultry hepatitis viruses in an effort to identify the knowledge gaps and aid the prevention and control of poultry viral hepatitis. Avian HEV is an Orthohepevirus B in the family Hepeviridae that naturally infects chickens and consists of three distinct genotypes worldwide. Avian HEV is associated with hepatitis-splenomegaly syndrome or big liver and spleen disease in chickens, although the majority of the infected birds are subclinical. Avihepadnaviruses in the family of Hepadnaviridae have been isolated from ducks, snow geese, white storks, grey herons, cranes, and parrots. DHBV evolved with the host as a noncytopathic form without clinical signs and rarely progressed to chronicity. The outcome for DHBV infection varies by the host's ability to elicit an immune response and is dose and age dependent in ducks, thus mimicking the pathogenesis of human hepatitis B virus (HBV) infections and providing an excellent animal model for human HBV. DHAV is a picornavirus that causes a highly contagious virus infection in ducks with up to 100% flock mortality in ducklings under 6 wk of age, while older birds remain unaffected. The high morbidity and mortality has an economic impact on intensive duck production farming. Duck hepatitis virus Types 2 and 3 are astroviruses in the family of Astroviridae with similarity phylogenetically to turkey astroviruses, implicating the potential for cross-species infections between strains. Duck astrovirus (DAstV) causes acute, fatal infections in ducklings with a rapid decline within 1-2 hr and clinical and pathologic signs virtually indistinguishable from DHAV. DAstV-1 has only been recognized in the United Kingdom and recently in China, while DAstV-2 has been reported in ducks in the United States. FAdV, the causative agent of inclusion body hepatitis, is a Group I avian adenovirus in the genus Aviadenovirus. The affected birds have a swollen, friable, and discolored liver, sometimes with necrotic or hemorrhagic foci. Histologic lesions include multifocal necrosis of hepatocytes and acute hepatitis with intranuclear inclusion bodies in the nuclei of the hepatocytes. THV is a picornavirus that is likely the causative agent of turkey viral hepatitis. Currently there are more questions than answers about THV, and the pathogenesis and clinical impacts remain largely unknown. Future research in viral hepatic diseases of poultry is warranted to develop specific diagnostic assays, identify suitable cell culture systems for virus propagation, and develop effective vaccines.
[Mh] Termos MeSH primário: Vírus de Hepatite/fisiologia
Hepatite Viral Animal
Doenças das Aves Domésticas
Aves Domésticas
[Mh] Termos MeSH secundário: Animais
Vírus de Hepatite/classificação
Hepatite Viral Animal/epidemiologia
Hepatite Viral Animal/transmissão
Hepatite Viral Animal/virologia
Doenças das Aves Domésticas/epidemiologia
Doenças das Aves Domésticas/transmissão
Doenças das Aves Domésticas/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170901
[Lr] Data última revisão:
170901
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160910
[St] Status:MEDLINE
[do] DOI:10.1637/11229-070515-Review.1


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Fotocópia
[PMID]:27483964
[Au] Autor:Takaoka A; Masuya A; Katsuyama N
[Ti] Título:[Pattern recognition receptor-mediated sensing mechanism during hepatitis virus infection].
[So] Source:Seikagaku;88(3):419-24, 2016 Jun.
[Is] ISSN:0037-1017
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Mh] Termos MeSH primário: Vírus de Hepatite/fisiologia
Hepatite Viral Humana/metabolismo
Receptores de Reconhecimento de Padrão/metabolismo
[Mh] Termos MeSH secundário: Animais
Hepatite Viral Humana/imunologia
Seres Humanos
Imunidade Inata
Integração Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Receptors, Pattern Recognition)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170410
[Lr] Data última revisão:
170410
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160804
[St] Status:MEDLINE



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