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Pesquisa : G06.920.925 [Categoria DeCS]
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  1 / 61831 MEDLINE  
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[PMID]:29438433
[Au] Autor:Oka T; Stoltzfus GT; Zhu C; Jung K; Wang Q; Saif LJ
[Ad] Endereço:Food Animal Health Research Program, Ohio Agricultural Research and Development Center, Department of Veterinary Preventive Medicine, The Ohio State University, Wooster, OH, United States of America.
[Ti] Título:Attempts to grow human noroviruses, a sapovirus, and a bovine norovirus in vitro.
[So] Source:PLoS One;13(2):e0178157, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Noroviruses (NoVs) and Sapoviruses (SaVs) are enteric caliciviruses that have been detected in multiple mammalian species, including humans. Currently, efficient cell culture systems have been established only for murine NoVs and porcine SaV Cowden strain. Establishment of an efficient in vitro cell culture system for other NoVs and SaVs remains challenging; however, human NoV (HuNoV) replication in 3D cultured Caco-2 cells and a clone of Caco-2 cells, C2BBe1, human enteroids and in human B cells has been reported. In this study, we tested various cells and culture conditions to grow HuNoVs and a human SaV (HuSaV) to test the possibility of the propagation in different cells and culture conditions. We also attempted to grow a bovine NoV (BoNoV) in ex vivo organ cultures. We did not observe significant RNA level increases for HuSaV and BoNoV under our test conditions. HuNoV RNA levels increased to a maximum of ~600-fold in long-term Caco-2 cells that were cultured for 1-2 months in multi-well plates and inoculated with HuNoV-positive and bacteria-free human stool suspensions using serum-free medium supplemented with the bile acid, GCDCA. However, this positive result was inconsistent. Our results demonstrated that HuNoVs, BoNoV and HuSaV largely failed to grow in vitro under our test conditions. Our purpose is to share our findings with other researchers with the goal to develop efficient, reproducible simplified and cost-effective culture systems for human and animal NoVs and SaVs in the future.
[Mh] Termos MeSH primário: Norovirus/fisiologia
Sapovirus/fisiologia
[Mh] Termos MeSH secundário: Células CACO-2
Seres Humanos
Técnicas In Vitro
Reação em Cadeia da Polimerase/métodos
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[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:180214
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0178157


  2 / 61831 MEDLINE  
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[PMID]:29373606
[Au] Autor:Devadas K; Biswas S; Ragupathy V; Lee S; Dayton A; Hewlett I
[Ad] Endereço:Laboratory of Molecular Virology, Division of Emerging and Transfusion Transmitted Diseases, Center for Biologics Evaluation and Research, Food and Drug Administration, Silver Spring, MD, United States of America.
[Ti] Título:Modulation of HIV replication in monocyte derived macrophages (MDM) by steroid hormones.
[So] Source:PLoS One;13(1):e0191916, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Significant sex specific differences in the progression of HIV/AIDS have been reported. Several studies have implicated steroid hormones in regulating host factor expression and modulating HIV transmission and replication. However, the exact mechanism exerted by steroid hormones estrogen and progesterone in the regulation of HIV-1 replication is still unclear. Results from the current study indicated a dose dependent down regulation of HIV-1 replication in monocyte derived macrophages pre-treated with high concentrations of estrogen or progesterone. To elucidate the molecular mechanisms associated with the down regulation of HIV-1 replication by estrogen and progesterone we used PCR arrays to analyze the expression profile of host genes involved in antiviral responses. Several chemokines, cytokines, transcription factors, interferon stimulated genes and genes involved in type-1 interferon signaling were down regulated in cells infected with HIV-1 pre-treated with high concentrations of estrogen or progesterone compared to untreated HIV-1 infected cells or HIV-1 infected cells treated with low concentrations of estrogen or progesterone. The down regulation of CXCL9, CXCL10 and CXCL11 chemokines and IL-1ß, IL-6 cytokines in response to high concentrations of estrogen and progesterone pre-treatment in HIV-1 infected cells was confirmed at the protein level by quantitating chemokine and cytokine concentrations in the culture supernatant. These results demonstrate that a potent anti-inflammatory response is mediated by pre-treatment with high concentrations of estrogen and progesterone. Thus, our study suggests a strong correlation between the down-modulation of anti-viral and pro-inflammatory responses mediated by estrogen and progesterone pre-treatment and the down regulation of HIV-1 replication. These findings may be relevant to clinical observations of sex specific differences in patient populations and point to the need for further investigation.
[Mh] Termos MeSH primário: Estrogênios/fisiologia
HIV/fisiologia
Macrófagos/virologia
Progesterona/fisiologia
Replicação Viral
[Mh] Termos MeSH secundário: Seres Humanos
Reação em Cadeia da Polimerase
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Estrogens); 4G7DS2Q64Y (Progesterone)
[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:180127
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191916


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[PMID]:29268134
[Au] Autor:Plebanek E; Lescrinier E; Andrei G; Snoeck R; Herdewijn P; De Jonghe S
[Ad] Endereço:Medicinal Chemistry, Rega Institute for Medical Research, KU Leuven, Herestraat 49 - bus 1041, 3000 Leuven, Belgium.
[Ti] Título:Emimycin and its nucleoside derivatives: Synthesis and antiviral activity.
[So] Source:Eur J Med Chem;144:93-103, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:The synthesis of emimycin, 5-substituted emimycin analogues and the corresponding ribo- and 2'-deoxyribonucleoside derivatives is described. Emimycin, its 5-substituted congeners and the ribonucleoside derivatives are completely devoid of antiviral activity against RNA viruses. In contrast, some of the 2'-deoxyribosyl emimycin derivatives are potent inhibitors of the replication of herpes simplex virus-1 and varicella-zoster virus, lacking cytotoxicity.
[Mh] Termos MeSH primário: Antivirais/química
Antivirais/farmacologia
Nucleosídeos/química
Nucleosídeos/farmacologia
Pirazinas/química
Pirazinas/farmacologia
[Mh] Termos MeSH secundário: Antivirais/síntese química
Linhagem Celular
Herpes Simples/tratamento farmacológico
Herpesvirus Humano 1/efeitos dos fármacos
Herpesvirus Humano 1/fisiologia
Herpesvirus Humano 3/efeitos dos fármacos
Herpesvirus Humano 3/fisiologia
Seres Humanos
Nucleosídeos/síntese química
Pirazinas/síntese química
Infecção pelo Vírus da Varicela-Zoster/tratamento farmacológico
Replicação Viral/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (Nucleosides); 0 (Pyrazines); R14TE35LHD (emimycin)
[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:171222
[St] Status:MEDLINE


  4 / 61831 MEDLINE  
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[PMID]:28456663
[Au] Autor:Singh S; Anupriya MG; Sreekumar E
[Ad] Endereço:Molecular Virology Laboratory, Rajiv Gandhi Centre for Biotechnology (RGCB), Thycaud P.O., Thiruvananthapuram 695014, Kerala, India.
[Ti] Título:Comparative whole genome analysis of dengue virus serotype-2 strains differing in trans-endothelial cell leakage induction in vitro.
[So] Source:Infect Genet Evol;52:34-43, 2017 Aug.
[Is] ISSN:1567-7257
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The role of genetic differences among dengue virus (DENV) in causing increased microvascular permeability is less explored. In the present study, we compared two closely related DENV serotype-2 strains of Cosmopolitan genotype for their in vitro infectivity phenotype and ability to induce trans-endothelial leakage. We found that these laboratory strains differed significantly in infecting human microvascular endothelial cells (HMEC-1) and hepatocytes (Huh7), two major target cells of DENV in in vivo infections. There was a reciprocal correlation in infectivity and vascular leakage induced by these strains, with the less infective strain inducing more trans-endothelial cell leakage in HMEC-1 monolayer upon infection. The cells infected with the strain capable of inducing more permeability were found to secrete more Non-Structural protein (sNS1) into the culture supernatant. A whole genome analysis revealed 37 predicted amino acid changes and changes in the secondary structure of 3' non-translated region between the strains. But none of these changes involved the signal sequence coded by the C-terminal of the Envelope protein and the two glycosylation sites within the NS1 protein critical for its secretion, and the N-terminal NS2A sequence important for surface targeting of NS1. The strain that secreted lower levels of NS1 and caused less leakage had two mutations within the NS1 protein coding region, F103S and T146I that significantly changed amino acid properties. A comparison of the sequences of the two strains with published sequences of various DENV strains known to cause clinically severe dengue identified a number of amino acid changes which could be implicated as possible key genetic differences. Our data supports the earlier observations that the vascular leakage induction potential of DENV strains is linked to the sNS1 levels. The results also indicate that viral genetic determinants, especially the mutations within the NS1 coding region, could affect this critical phenotype of DENV strains.
[Mh] Termos MeSH primário: Vírus da Dengue/fisiologia
Células Endoteliais/virologia
Hepatócitos/virologia
Proteínas não Estruturais Virais/genética
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Animais
Permeabilidade Capilar
Linhagem Celular
Vírus da Dengue/genética
Células Endoteliais/citologia
Variação Genética
Genoma Viral
Hepatócitos/citologia
Seres Humanos
Estrutura Secundária de Proteína
Análise de Sequência de RNA
Proteínas não Estruturais Virais/química
Proteínas não Estruturais Virais/secreção
Replicação Viral/fisiologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (NS1 protein, Dengue virus type 2); 0 (Viral Nonstructural Proteins)
[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:170501
[St] Status:MEDLINE


  5 / 61831 MEDLINE  
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[PMID]:29458547
[Au] Autor:Growcott EJ; Bamba D; Galarneau JR; Leonard VHJ; Schul W; Stein D; Osborne CS
[Ad] Endereço:1​Novartis Institutes for Biomedical Research, Infectious Disease, Emeryville, CA, USA.
[Ti] Título:The effect of P38 MAP kinase inhibition in a mouse model of influenza.
[So] Source:J Med Microbiol;67(3):452-462, 2018 Mar.
[Is] ISSN:1473-5644
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Influenza viruses are a common cause of human respiratory infections, resulting in epidemics of high morbidity and mortality. We investigated the effect of a novel mitogen-activated protein kinase (MAPK) inhibitor in vitro and in a murine influenza model to further explore whether p38 MAPK inhibition could reduce viral replication. METHODS: In vitro, the antiviral effect of p38 MAPK inhibitor BCT194 was evaluated in differentiated human bronchial epithelial cells (HBECs); in vivo, female BALB/c mice were infected intranasally with 150 pfu of influenza H1N1 A/Puerto Rico/8/34 and treated with BCT197 (a closely related p38 MAPK inhibitor with an IC50 value of<1 µM, currently in clinical testing), dexamethasone or oseltamivir (Tamiflu) starting 24 h post infection. Body weight, bronchoalveolar lavage cells, cytokines, total protein and lactate dehydrogenase as well as serum cytokines were measured; a subset of animals was evaluated histopathologically.Results/Key findings. p38MAP kinase inhibition with BCT194 had no impact on influenza replication in HBECs. When examining BCT197 in vivo, and comparing to vehicle-treated animals, reduced weight loss, improvement in survival and lack of impaired viral control was observed at BCT197 concentrations relevant to those being used in clinical trials of acute exacerbations of chronic obstructive pulmonary disease; at higher concentrations of BCT197 these effects were reduced. CONCLUSIONS: Compared to vehicle treatment, BCT197 (administered at a clinically relevant concentration) improved outcomes in a mouse model of influenza. This is encouraging given that the use of innate inflammatory pathway inhibitors may raise concerns of negative effects on infection regulation.
[Mh] Termos MeSH primário: Antivirais/farmacologia
Inibidores Enzimáticos/farmacologia
Vírus da Influenza A Subtipo H1N1/efeitos dos fármacos
Infecções por Orthomyxoviridae/virologia
Proteínas Quinases p38 Ativadas por Mitógeno/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Antivirais/administração & dosagem
Antivirais/uso terapêutico
Brônquios/citologia
Linhagem Celular
Citocinas/sangue
Dexametasona/uso terapêutico
Modelos Animais de Doenças
Inibidores Enzimáticos/administração & dosagem
Inibidores Enzimáticos/uso terapêutico
Células Epiteliais/efeitos dos fármacos
Células Epiteliais/virologia
Feminino
Seres Humanos
Vírus da Influenza A Subtipo H1N1/fisiologia
Influenza Humana/tratamento farmacológico
Influenza Humana/virologia
Camundongos
Camundongos Endogâmicos BALB C
Infecções por Orthomyxoviridae/tratamento farmacológico
Oseltamivir/uso terapêutico
Resultado do Tratamento
Replicação Viral/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (Cytokines); 0 (Enzyme Inhibitors); 20O93L6F9H (Oseltamivir); 7S5I7G3JQL (Dexamethasone); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180221
[St] Status:MEDLINE
[do] DOI:10.1099/jmm.0.000684


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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


  7 / 61831 MEDLINE  
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[PMID]:29388837
[Au] Autor:Martinez-Jaramillo E; Garza-Morales R; Wechman SL; Montes de Oca-Luna R; Saucedo-Cardenas O; Shirwan H; Yolcu E; McMasters KM; Gomez-Gutierrez JG
[Ad] Endereço:a The Hiram C. Polk Jr., MD, Department of Surgery , University of Louisville School of Medicine , Louisville , USA.
[Ti] Título:Adenovirus Lacking E1b Efficiently Induces Cytopathic Effect in HPV-16-Positive Murine Cancer Cells via Virus Replication and Apoptosis.
[So] Source:Cancer Invest;36(1):19-27, 2018 Jan 02.
[Is] ISSN:1532-4192
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Conditionally replicative adenoviruses (CRAds) replicate poorly in murine cancer cells; however, E1b-deleted CRAds may replicate effectively in HPV16-E6/E7-positive murine cancer cells (TC-1). The HPV16 E7 open reading frame encodes functions analogous to these deleted adenovirus E1 proteins. In this study, an E1b-deleted CRAd (Adhz60) was evaluated for its ability to replicate and induce oncolysis in TC-1 cells. Adhz60-mediated oncolysis was similar in TC-1 and HeLa cells. Productive viral replication was evident based on expression of E1A and hexon, production of infectious virus progeny, and Adhz60-induced apoptosis. The results suggest that TC-1 murine cancer cells allow Adhz60 replication and oncolysis.
[Mh] Termos MeSH primário: Adenoviridae/genética
Proteínas E1B de Adenovirus/genética
Apoptose/genética
Papillomavirus Humano 16/genética
Replicação Viral/genética
[Mh] Termos MeSH secundário: Animais
Apoptose/fisiologia
Linhagem Celular Tumoral
Células HEK293
Células HeLa
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Proteínas Oncogênicas Virais/genética
Proteínas E7 de Papillomavirus/genética
Proteínas Repressoras/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adenovirus E1B Proteins); 0 (E6 protein, Human papillomavirus type 16); 0 (Oncogene Proteins, Viral); 0 (Papillomavirus E7 Proteins); 0 (Repressor Proteins); 0 (oncogene protein E7, Human papillomavirus type 16)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180202
[St] Status:MEDLINE
[do] DOI:10.1080/07357907.2018.1430812


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[PMID]:29302027
[Au] Autor:Campbell M; Watanabe T; Nakano K; Davis RR; Lyu Y; Tepper CG; Durbin-Johnson B; Fujimuro M; Izumiya Y
[Ad] Endereço:Department of Dermatology, School of Medicine, University of California Davis (UC Davis), Sacramento, CA, 95817, USA.
[Ti] Título:KSHV episomes reveal dynamic chromatin loop formation with domain-specific gene regulation.
[So] Source:Nat Commun;9(1):49, 2018 01 04.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The three-dimensional structure of chromatin organized by genomic loops facilitates RNA polymerase II access to distal promoters. The Kaposi's sarcoma-associated herpesvirus (KSHV) lytic transcriptional program is initiated by a single viral transactivator, K-Rta. Here we report the KSHV genomic structure and its relationship with K-Rta recruitment sites using Capture Hi-C analyses. High-resolution 3D viral genomic maps identify a number of direct physical, long-range, and dynamic genomic interactions. Mutant KSHV chromosomes harboring point mutations in the K-Rta responsive elements (RE) significantly attenuate not only the directly proximate downstream gene, but also distal gene expression in a domain-specific manner. Genomic loops increase in the presence of K-Rta, while abrogation of K-Rta binding impairs the formation of inducible genomic loops, decreases the expression of genes networked through the looping, and diminishes KSHV replication. Our study demonstrates that genomic architectural dynamics plays an essential role in herpesvirus gene expression.
[Mh] Termos MeSH primário: Regulação Viral da Expressão Gênica
Genoma Viral/genética
Herpesvirus Humano 8/genética
Plasmídeos/genética
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Linhagem Celular Tumoral
Cercopithecus aethiops
Seres Humanos
Transativadores/genética
Células Vero
Proteínas Virais/genética
Latência Viral/genética
Replicação Viral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Trans-Activators); 0 (Viral Proteins)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180106
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02089-9


  9 / 61831 MEDLINE  
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[PMID]:28464845
[Au] Autor:Wei X; Li N; Li S; Shi J; Guo W; Zheng Y; Cheng S
[Ad] Endereço:Department of Hepatic Surgery VI, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, 225 Changhai Road, Yangpu District, Shanghai, 200438, China.
[Ti] Título:Hepatitis B virus infection and active replication promote the formation of vascular invasion in hepatocellular carcinoma.
[So] Source:BMC Cancer;17(1):304, 2017 May 02.
[Is] ISSN:1471-2407
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Vascular invasion, including microvascular invasion (MVI) and portal vein tumor thrombus (PVTT), is associated with the postoperative recurrence of hepatocellular carcinoma (HCC). We aimed to investigate the potential impact of hepatitis B virus (HBV) activity on the development of vascular invasion. METHODS: Patients with HBV and tumor-related factors of HCC who had undergone hepatectomy were retrospectively enrolled and analyzed to identify the risk factors for developing vascular invasion. RESULTS: A total of 486 patients were included in this study. The overall proportion of patients with vascular invasion, including MVI and PVTT, was 60.3% (293/486). The incidence of MVI was 58.2% (283/486) whereas PVTT was 22.2% (108/486). Univariate analysis revealed that positive Hepatitis B virus surface Antigen (HBsAg) was significantly associated with the presence of vascular invasion. In a multivariate regression analysis carried out in patients with HBV-related HCC, positive Hepatitis B virus e Antigen (HBeAg)(OR = 1.83, P = 0.019) and a detectable seral HBV DNA load (OR = 1.68, P = 0.027) were independent risk factors of vascular invasion. The patients in the severe MVI group had a significantly higher rate of positive seral HBsAg (P = 0.005), positive seral HBeAg (P = 0.016), a detectable seral HBV DNA load (> 50 IU/ml) (P < 0.001) and a lower rate of anti-viral treatment (P = 0.002) compared with those in the mild MVI group and MVI-negative group. Whereas, HCC with PVTT invading the main trunk showed a significantly higher rate of positive HBsAg (P = 0.007), positive HBeAg (P = 0.04), cirrhosis (P = 0.005) and a lower rate of receiving antiviral treatment (P = 0.009) compared with patients with no PVTT or PVTT invading the ipsilateral portal vein. Patients with vascular invasion also had a significantly higher level of seral HBV DNA load than patients without vascular invasion (P = 0.008). CONCLUSIONS: In HCC patients, HBV infection and active HBV replication were associated with the development of vascular invasion.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular
Vírus da Hepatite B
Hepatite B
Neoplasias Hepáticas
Neovascularização Patológica
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Antivirais/uso terapêutico
Feminino
Seres Humanos
Masculino
Meia-Idade
Estudos Retrospectivos
Replicação Viral
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiviral Agents)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1186/s12885-017-3293-6


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[PMID]:28460470
[Au] Autor:Cheng T; Song Y; Zhang Y; Zhang C; Yin J; Chi Y; Zhou D
[Ad] Endereço:Vaccine Research Center, Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Science, Shanghai 200031, China.
[Ti] Título:A novel oncolytic adenovirus based on simian adenovirus serotype 24.
[So] Source:Oncotarget;8(16):26871-26885, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Among the oncolytic virotherapy, an emerging treatment for tumor, adenoviruses are widely used at present in preclinical and clinical trials. Traditionally, oncolytic adenoviruses were developed based on the human adenovirus serotype 5 (AdHu5). However, AdHu5 has the drawbacks of preexisting anti-AdHu5 immunity in most populations, and extensive sequestration of Adhu5 by the liver through hexon, blood coagulation factor X (FX), and FX receptor interactions. To tackle these problems, we explored a novel oncolytic adenovirus AdC7-SP/E1A-ΔE3 for cancer treatment. AdC7-SP/E1A-ΔE3 was constructed by replacing the E1A promoter with tumor specific promoter survivin promoter and deleting E3 region using direct cloning methods based on simian adenovirus serotype 24 (namely AdC7). We showed that AdC7-SP/E1A-ΔE3 significantly killed tumor cell lines NCI-H508 and Huh7, and inhibited tumor growth in both NCI-H508 and Huh7 xenograft tumor models. Importantly, AdC7-SP/E1A-ΔE3 exhibited the antitumor efficacy via systemic administration. Mechanistically, infected cells were killed by AdC7-SP/E1A-ΔE3 via the p53-independent mitochondrial apoptosis pathway in which phosphorylation of BAD markedly declined and the expresses of Bik significantly went up. Therefore, AdC7-SP/E1A-ΔE3 is a promising candidate for liver and colon tumor treatment.
[Mh] Termos MeSH primário: Adenovirus dos Símios/classificação
Adenovirus dos Símios/genética
Vetores Genéticos/genética
Vírus Oncolíticos/genética
[Mh] Termos MeSH secundário: Proteínas E1A de Adenovirus/genética
Animais
Apoptose/genética
Linhagem Celular Tumoral
Efeito Citopatogênico Viral
Modelos Animais de Doenças
Deleção de Genes
Expressão Gênica
Engenharia Genética
Terapia Genética
Vetores Genéticos/administração & dosagem
Vetores Genéticos/efeitos adversos
Seres Humanos
Proteínas Inibidoras de Apoptose/genética
Camundongos
Mitocôndrias/genética
Terapia Viral Oncolítica
Especificidade de Órgãos/genética
Regiões Promotoras Genéticas
Sorogrupo
Transdução de Sinais
Carga Tumoral
Proteína Supressora de Tumor p53/genética
Proteína Supressora de Tumor p53/metabolismo
Replicação Viral
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adenovirus E1A Proteins); 0 (BIRC5 protein, human); 0 (Inhibitor of Apoptosis Proteins); 0 (Tumor Suppressor Protein p53)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15845



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