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[PMID]:28794032
[Au] Autor:Bamunusinghe D; Liu Q; Plishka R; Dolan MA; Skorski M; Oler AJ; Yedavalli VRK; Buckler-White A; Hartley JW; Kozak CA
[Ad] Endereço:Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland, USA.
[Ti] Título:Recombinant Origins of Pathogenic and Nonpathogenic Mouse Gammaretroviruses with Polytropic Host Range.
[So] Source:J Virol;91(21), 2017 Nov 01.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ecotropic, xenotropic, and polytropic mouse leukemia viruses (E-, X-, and P-MLVs) exist in mice as infectious viruses and endogenous retroviruses (ERVs) inserted into mouse chromosomes. All three MLV subgroups are linked to leukemogenesis, which involves generation of recombinants with polytropic host range. Although P-MLVs are deemed to be the proximal agents of disease induction, few biologically characterized infectious P-MLVs have been sequenced for comparative analysis. We analyzed the complete genomes of 16 naturally occurring infectious P-MLVs, 12 of which were typed for pathogenic potential. We sought to identify ERV progenitors, recombinational hot spots, and segments that are always replaced, never replaced, or linked to pathogenesis or host range. Each P-MLV has an E-MLV backbone with P- or X-ERV replacements that together cover 100% of the recombinant genomes, with different substitution patterns for X- and P-ERVs. Two segments are always replaced, both coding for envelope (Env) protein segments: the N terminus of the surface subunit and the cytoplasmic tail R peptide. Viral gene replacements are influenced by host restriction genes and Pathogenic potential maps to the transmembrane subunit segment encoding the N-heptad repeat (HR1). Molecular dynamics simulations identified three novel interdomain salt bridges in the lymphomagenic virus HR1 that could affect structural stability, entry or sensitivity to host immune responses. The long terminal repeats of lymphomagenic P-MLVs are differentially altered by recombinations, duplications, or mutations. This analysis of the naturally occurring, sometimes pathogenic P-MLV recombinants defines the limits and extent of intersubgroup recombination and identifies specific sequence changes linked to pathogenesis and host interactions. During virus-induced leukemogenesis, ecotropic mouse leukemia viruses (MLVs) recombine with nonecotropic endogenous retroviruses (ERVs) to produce polytropic MLVs (P-MLVs). Analysis of 16 P-MLV genomes identified two segments consistently replaced: one at the envelope N terminus that alters receptor choice and one in the R peptide at the envelope C terminus, which is removed during virus assembly. Genome-wide analysis shows that nonecotropic replacements in the progenitor ecotropic MLV genome are more extensive than previously appreciated, covering 100% of the genome; contributions from xenotropic and polytropic ERVs differentially alter the regions responsible for receptor determination or subject to APOBEC3 and Fv1 restriction. All pathogenic viruses had modifications in the regulatory elements in their long terminal repeats and differed in a helical segment of envelope involved in entry and targeted by the host immune system. Virus-induced leukemogenesis thus involves generation of complex recombinants, and specific replacements are linked to pathogenesis and host restrictions.
[Mh] Termos MeSH primário: Especificidade de Hospedeiro/genética
Vírus da Leucemia Murina/classificação
Vírus da Leucemia Murina/patogenicidade
Leucemia Experimental/virologia
Infecções por Retroviridae/virologia
Infecções Tumorais por Vírus/virologia
Proteínas Virais/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Sequência de Bases
Evolução Molecular
Genoma Viral
Vírus da Leucemia Murina/genética
Camundongos
Simulação de Dinâmica Molecular
Conformação Proteica
Receptores Virais/genética
Receptores Virais/metabolismo
Homologia de Sequência
Sequências Repetidas Terminais
Proteínas Virais/química
Proteínas Virais/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Virus); 0 (Viral Proteins)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170811
[St] Status:MEDLINE


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[PMID]:28687662
[Au] Autor:Zhang C; He H; Wang L; Zhang N; Huang H; Xiong Q; Yan Y; Wu N; Ren H; Han H; Liu M; Qian M; Du B
[Ad] Endereço:Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai 200241, China; and.
[Ti] Título:Virus-Triggered ATP Release Limits Viral Replication through Facilitating IFN-ß Production in a P2X7-Dependent Manner.
[So] Source:J Immunol;199(4):1372-1381, 2017 Aug 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Accumulating evidence shows that innate immune responses are associated with extracellular nucleotides, particularly ATP. In this article, we demonstrate extensive protection of ATP/P2X7 signaling in a host against viral infection. Interestingly, we observed a significant increase in ATP as a danger signal in vesicular stomatitis virus (VSV)-infected cell supernatant and VSV-infected mice in an exocytosis- and pannexin channel-dependent manner. Furthermore, extracellular ATP reduces the replication of VSV, Newcastle disease virus, murine leukemia virus, and HSV in vivo and in vitro through the P2X7 receptor. Meanwhile, ATP significantly increases IFN-ß expression in a concentration- and time-dependent manner. Mechanistically, ATP facilitates IFN-ß secretion through P38/JNK/ATF-2 signaling pathways, which are crucial in promoting antiviral immunity. Taken together, these results demonstrate the protective role of extracellular ATP and P2X7 in viral infection and suggest a potential therapeutic role for ATP/P2X7 in viral diseases.
[Mh] Termos MeSH primário: Trifosfato de Adenosina/metabolismo
Interferon beta/biossíntese
Receptores Purinérgicos P2X7/metabolismo
Estomatite Vesicular/imunologia
Vírus da Estomatite Vesicular Indiana/fisiologia
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/farmacologia
Animais
Imunidade Inata
Interferon beta/genética
Interferon beta/imunologia
Vírus da Leucemia Murina/efeitos dos fármacos
Vírus da Leucemia Murina/imunologia
Medições Luminescentes
Camundongos
Vírus da Doença de Newcastle/efeitos dos fármacos
Vírus da Doença de Newcastle/imunologia
Células RAW 264.7
Receptores Purinérgicos P2X7/imunologia
Transdução de Sinais
Simplexvirus/efeitos dos fármacos
Simplexvirus/imunologia
Estomatite Vesicular/virologia
Vírus da Estomatite Vesicular Indiana/efeitos dos fármacos
Vírus da Estomatite Vesicular Indiana/imunologia
Replicação Viral/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Purinergic P2X7); 77238-31-4 (Interferon-beta); 8L70Q75FXE (Adenosine Triphosphate)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170709
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700187


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[PMID]:28315663
[Au] Autor:Jaguva Vasudevan AA; Hofmann H; Willbold D; Häussinger D; Koenig BW; Münk C
[Ad] Endereço:Clinic for Gastroenterology, Hepatology, and Infectiology, Medical Faculty, Heinrich-Heine-University Düsseldorf, Moorenstr. 5, 40225 Düsseldorf, Germany.
[Ti] Título:Enhancing the Catalytic Deamination Activity of APOBEC3C Is Insufficient to Inhibit Vif-Deficient HIV-1.
[So] Source:J Mol Biol;429(8):1171-1191, 2017 Apr 21.
[Is] ISSN:1089-8638
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The retroviral restriction factors of the APOBEC3 (A3) cytidine deaminase family catalyze the deamination of cytidines in single-stranded viral DNA. APOBEC3C (A3C) is a strong antiviral factor against viral infectivity factor (vif)-deficient simian immunodeficiency virus Δvif, which is, however, a weak inhibitor against human immunodeficiency virus (HIV)-1 for reasons unknown. The precise link between the antiretroviral effect of A3C and its catalytic activity is incompletely understood. Here, we show that the S61P mutation in human A3C (A3C.S61P) boosted hypermutation in the viral genomes of simian immunodeficiency virus Δvif and murine leukemia virus but not in human immunodeficiency virus HIV-1Δvif. The enhanced antiviral activity of A3C.S61P correlated with enhanced in vitro cytidine deamination. Furthermore, the S61P mutation did not change the substrate specificity of A3C, ribonucleoprotein complex formation, self-association, Zinc coordination, or viral incorporation features. We propose that local structural changes induced by the serine-to-proline substitution are responsible for the gain of catalytic activity of A3C.S61P. Our results are a first step toward an understanding of A3C's DNA binding capacity, deamination-dependent editing, and antiviral functions at the molecular level. We conclude that the enhanced enzymatic activity of A3C is insufficient to restrict HIV-1, indicating an unknown escape mechanism of HIV-1.
[Mh] Termos MeSH primário: Citidina Desaminase/química
Citidina Desaminase/metabolismo
HIV-1/patogenicidade
[Mh] Termos MeSH secundário: Substituição de Aminoácidos
Animais
Citidina Desaminase/genética
Citosina/metabolismo
DNA de Cadeia Simples/química
DNA de Cadeia Simples/metabolismo
DNA Viral/metabolismo
Células HEK293/virologia
HIV-1/genética
Interações Hospedeiro-Patógeno
Seres Humanos
Vírus da Leucemia Murina/metabolismo
Vírus da Leucemia Murina/patogenicidade
Pan troglodytes
Conformação Proteica
Vírus da Imunodeficiência Símia/metabolismo
Vírus da Imunodeficiência Símia/patogenicidade
Zinco/metabolismo
Produtos do Gene vif do Vírus da Imunodeficiência Humana/genética
Produtos do Gene vif do Vírus da Imunodeficiência Humana/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Single-Stranded); 0 (DNA, Viral); 0 (vif Gene Products, Human Immunodeficiency Virus); 0 (vif protein, Human immunodeficiency virus 1); 8J337D1HZY (Cytosine); EC 3.5.4.5 (APOBEC3C protein, human); EC 3.5.4.5 (Cytidine Deaminase); J41CSQ7QDS (Zinc)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170427
[Lr] Data última revisão:
170427
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170320
[St] Status:MEDLINE


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[PMID]:28292718
[Au] Autor:Boi S; Dis EV; Hansen EJ; Rosenke K; Peterson KE; Ferrell ME; Evans LH
[Ad] Endereço:Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, Hamilton, Montana 59840 United States.
[Ti] Título:Latent murine leukemia virus infection characterized by the release of non-infectious virions.
[So] Source:Virology;506:19-27, 2017 Jun.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Clonal cell lines derived from cultures infected with a polytropic MuLV release vastly different levels of infectious virions ranging from undetectable to very high. Low producing clones release an overwhelming proportion of non-infectious virions containing retroviral RNA but deficient in the Env protein. Non-infectious virion production is not due to an inability of the cells to support infectious MuLV production or to an inherent replicative defectiveness of the proviruses. Reinfection of the lowest producing lines with the polytropic or an ecotropic MuLV results in enormous increases in the specific infectivity of the released virions. This indicates a reversible state of retroviral latency characterized by the release of non-infectious virions that is likely the result of insufficient levels of Env protein required for infectivity. The latency state described here may have important roles in in vivo retroviral infections including alterations of the immune response and the production of defective interfering particles.
[Mh] Termos MeSH primário: Vírus da Leucemia Murina/fisiologia
Infecções por Retroviridae/virologia
Vírion/fisiologia
Latência Viral
Liberação de Vírus
[Mh] Termos MeSH secundário: Animais
Produtos do Gene env/genética
Produtos do Gene env/metabolismo
Seres Humanos
Vírus da Leucemia Murina/genética
Camundongos
Vírion/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gene Products, env)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170705
[Lr] Data última revisão:
170705
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170316
[St] Status:MEDLINE


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[PMID]:28250122
[Au] Autor:Opazo T; Garcés A; Tapia D; Barraza F; Bravo A; Schwenke T; Cancino J; Arriagada G
[Ad] Endereço:Departamento de Ciencias Biologicas, Facultad de Ciencias Biologicas, Universidad Andres Bello, Viña del Mar, Chile.
[Ti] Título:Functional Evidence of the Involvement of the Dynein Light Chain DYNLRB2 in Murine Leukemia Virus Infection.
[So] Source:J Virol;91(10), 2017 May 15.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:How murine leukemia virus (MLV) travels from the cell membrane to the nucleus and the mechanism for nuclear entry of MLV DNA in dividing cells still remain unclear. It seems likely that the MLV preintegration complex (PIC) interacts with cellular proteins to perform these tasks. We recently published that the microtubule motor cytoplasmic dynein complex and its regulator proteins interact with the MLV PIC at early times of infection, suggesting a functional interaction between the incoming viral particles, the dynein complex, and dynein regulators. To better understand the role of the dynein complex in MLV infection, we performed short hairpin RNA (shRNA) screening of the dynein light chains on MLV infection. We found that silencing of a specific light chain of the cytoplasmic dynein complex, DYNLRB2, reduced the efficiency of infection by MLV reporter viruses without affecting HIV-1 infection. Furthermore, the overexpression of DYNLRB2 increased infection by MLV. We conclude that the DYNLRB2 light chain of the cytoplasmic dynein complex is an important and specific piece of the host machinery needed for MLV infection. Retroviruses must reach the chromatin of their host to integrate their viral DNA, but first they must get into the nucleus. The cytoplasm is a crowded environment in which simple diffusion is slow, and thus viruses utilize retrograde transport along the microtubule network, mediated by the dynein complex. Different viruses use different components of this multisubunit complex. We have found that murine leukemia virus (MLV) associates functionally and specifically with the dynein light chain DYNLRB2, which is required for infection. Our study provides more insight into the molecular requirements for retrograde transport of the MLV preintegration complex and demonstrates, for the first time, a role for DYNLRB2 in viral infection.
[Mh] Termos MeSH primário: Dineínas do Citoplasma/genética
Dineínas do Citoplasma/fisiologia
Interações Hospedeiro-Patógeno
Vírus da Leucemia Murina/fisiologia
[Mh] Termos MeSH secundário: Animais
Transporte Biológico
Linhagem Celular
Núcleo Celular/virologia
Células HEK293
HIV-1/fisiologia
Interações Hospedeiro-Patógeno/genética
Seres Humanos
Camundongos
Microtúbulos/virologia
Células NIH 3T3
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.6.4.2 (Cytoplasmic Dyneins); EC 3.6.4.2 (DYNLRB2 protein, human)
[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:170303
[St] Status:MEDLINE


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[PMID]:28028680
[Au] Autor:Li YJ; ZhuGe FY; Zeng CC; He JY; Tan N; Liang J
[Ad] Endereço:School of Biomedical Technology, Guilin Medical University, No. 109, North 2nd Ring Road, Guilin, 541004, Guangxi, China.
[Ti] Título:Establishment of mouse leukemia cell lines expressing human CD4/CCR5 using lentiviral vectors.
[So] Source:Virus Genes;53(2):197-204, 2017 Apr.
[Is] ISSN:1572-994X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A low-cost rodent model of HIV infection and which presents high application value is an effective tool to investigate HIV infection and pathogenesis. However, development of such a small animal model has been hampered by the unsuitability of rodent cells for HIV-1 replication given that the retrovirus HIV-1 has high selectivity to its host cell. Our study used the mouse leukemia cell lines L615 and L1210 that were induced by murine leukemia virus and transfected with hCD4/CCR5 loaded-lentiviral vector. Lentiviral vectors containing the genes hCD4/CCR5 under the transcriptional control of cytomegalovirus promoter were designed. Transfection efficiencies of human CD4 and CCR5 in L615 and L1210 cells were analyzed by quantitative real-time polymerase chain reaction (RT-PCR) and Western blot assay. Results showed that hCD4 and CCR5 proteins were expressed on the cell surface, demonstrating that the L615 and L1210 cells were humanized and that they possess the characteristics necessary for HIV infection of human host cells. Moreover, the sensitivity of human CD4/CCR5 transgenic mouse cells to HIV infection was confirmed by RT-PCR and ELISA. Mouse leukemia cell lines that could express hCD4 and CCR5 were thus established to facilitate normal entry of HIV-1 so that a human CD4/CCR5 transgenic mice cell model can be used to investigate the transmission and pathogenesis of HIV/AIDS and potential antiviral drugs against this disease.
[Mh] Termos MeSH primário: Antígenos CD4/biossíntese
Infecções por HIV/genética
Vírus da Leucemia Murina/genética
Receptores CCR5/biossíntese
[Mh] Termos MeSH secundário: Animais
Antígenos CD4/genética
Modelos Animais de Doenças
Regulação Viral da Expressão Gênica
Vetores Genéticos
Infecções por HIV/tratamento farmacológico
Infecções por HIV/virologia
HIV-1/genética
HIV-1/patogenicidade
Seres Humanos
Lentivirus/genética
Camundongos
Camundongos Transgênicos
Receptores CCR5/genética
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCR5 protein, human); 0 (CD4 Antigens); 0 (Receptors, CCR5)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161229
[St] Status:MEDLINE
[do] DOI:10.1007/s11262-016-1423-x


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[PMID]:27800626
[Au] Autor:Conley L; Tao Y; Henry A; Koepf E; Cecchini D; Pieracci J; Ghose S
[Ad] Endereço:Process Biochemistry, Biogen, 5000 Davis Drive, Research Triangle Park 27709, North Carolina.
[Ti] Título:Evaluation of eco-friendly zwitterionic detergents for enveloped virus inactivation.
[So] Source:Biotechnol Bioeng;114(4):813-820, 2017 Apr.
[Is] ISSN:1097-0290
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Inclusion of a detergent in protein biotherapeutic purification processes is a simple and very robust method for inactivating enveloped viruses. The detergent Triton X-100 has been used for many years and is part of the production process of several commercial therapeutic proteins. However, recent ecological studies have suggested that Triton X-100 and its break-down products can potentially behave as endocrine disrupters in aquatic organisms, raising concerns from an environmental impact perspective. As such, discharge of Triton X-100 into the waste water treatment plants is regulated in some jurisdictions, and alternative detergents for viral inactivation are required. In this work, we report on the identification and evaluation of more eco-friendly detergents as viable replacements for Triton X-100. Five detergent candidates with low to moderate environmental impact were initially identified and evaluated with respect to protein stability, followed by proof-of-concept virus inactivation studies using a model enveloped virus. From the set of candidates lauryldimethylamine N-oxide (LDAO) was identified as the most promising detergent due to its low ecotoxicity, robust anti-viral activity (LRV >4 at validation set-point conditions with X-MuLX), and absence of any negative impact on protein function. This detergent exhibited effective and robust virus inactivation in a broad range of protein concentrations, solution conductivities, pHs, and in several different cell culture fluid matrices. The only process parameter which correlated with reduced virus inactivation potency was LDAO concentration, and then only when the concentration was reduced to below the detergent's critical micelle concentration (CMC). Additionally, this work also demonstrated that LDAO was cleared to below detectable levels after Protein A affinity chromatography, making it suitable for use in a platform process that utilizes this chromatographic mode for protein capture. All these findings suggest that LDAO may be a practical alternative to Triton X-100 for use in protein therapeutic production processes for inactivating enveloped viruses. Biotechnol. Bioeng. 2017;114: 813-820. © 2016 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Detergentes/química
Detergentes/farmacologia
Dimetilaminas/química
Dimetilaminas/farmacologia
Inativação de Vírus/efeitos dos fármacos
[Mh] Termos MeSH secundário: Química Verde
Herpesvirus Suídeo 1/efeitos dos fármacos
Vírus da Leucemia Murina/efeitos dos fármacos
Modelos Moleculares
Octoxinol/química
Octoxinol/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Detergents); 0 (Dimethylamines); 4F6FC4MI8W (dodecyldimethylamine oxide); 9002-93-1 (Octoxynol)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161102
[St] Status:MEDLINE
[do] DOI:10.1002/bit.26209


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[PMID]:27721401
[Au] Autor:Tsuruyama T; Hiratsuka T; Yamada N
[Ad] Endereço:Department of Pathology, Kyoto University, Graduate School of Medicine, Sakyo-ku, Kyoto, Japan.
[Ti] Título:Hotspots of MLV integration in the hematopoietic tumor genome.
[So] Source:Oncogene;36(9):1169-1175, 2017 Mar 02.
[Is] ISSN:1476-5594
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Extensive research has been performed regarding the integration sites of murine leukemia retrovirus (MLV) for the identification of proto-oncogenes. To date, the overlap of mutations within specific oligonucleotides across different tumor genomes has been regarded as a rare event; however, a recent study of MLV integration into the oncogene Zfp521 suggested the existence of a hotspot oligonucleotide for MLV integration. In the current review, we discuss the hotspots of MLV integration into several genes: c-Myc, Stat5a and N-myc, as well as ZFP521, as examined in tumor genomes. From this, MLV integration convergence within specific oligonucleotides is not necessarily a rare event. This short review aims to promote re-consideration of MLV integration within the tumor genome, which involves both well-known and potentially newly identified and novel mechanisms and specifications.
[Mh] Termos MeSH primário: Genoma Humano
Neoplasias Hematológicas/genética
Vírus da Leucemia Murina/genética
Integração Viral/genética
[Mh] Termos MeSH secundário: Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[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:161011
[St] Status:MEDLINE
[do] DOI:10.1038/onc.2016.285


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[PMID]:27620499
[Au] Autor:Ellgaard TW; Bindslev L; Kamstrup S
[Ad] Endereço:Dept. 609, Biopharm Purification Development & Virology, Novo Nordisk A/S, Hagedornsvej 1, DK-2820 Gentofte, Denmark. Electronic address: tryw@novonordisk.com.
[Ti] Título:Evaluation of the virus clearance capacity and robustness of the manufacturing process for the recombinant factor VIII protein, turoctocog alfa.
[So] Source:Protein Expr Purif;129:94-100, 2017 Jan.
[Is] ISSN:1096-0279
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Turoctocog alfa is a B-domain-truncated recombinant factor VIII protein produced in a Chinese hamster ovary (CHO) cell line. The aim of this study was to evaluate the virus clearance capacity and robustness of the turoctocog alfa purification process. Virus clearance evaluation studies were conducted utilising a scaled-down version of the manufacturing process. Total virus clearance was evaluated using the ecotropic murine leukaemia virus (eMuLV) as a model for non-infectious retrovirus-like particles (RVLPs) and certain enveloped viruses. Other viruses utilised included: infectious bovine rhinotracheitis (IBRV), minute virus of mice (MVM), bovine enterovirus (BEV) and Reo-3 virus (Reo-3). Robust clearance of all model viruses was demonstrated with either new or reused resins. Overall, virus reduction factors were: >18.0 log (eMuLV); 11.0 log (MVM); >11.8 log (Reo-3; >5.0 log using nanofiltration); >15.3 log (BEV) and >12.7 log (IBRV). Taken together, these values demonstrate that the purification process for turoctocog alfa effectively removes a range of enveloped and non-enveloped viruses of different physicochemical properties and sizes.
[Mh] Termos MeSH primário: Enterovirus Bovino
Fator VIII/isolamento & purificação
Herpesvirus Bovino 1
Vírus da Leucemia Murina
Vírus Miúdo do Camundongo
Inativação de Vírus
[Mh] Termos MeSH secundário: Animais
Células CHO
Bovinos
Cricetinae
Cricetulus
Fator VIII/biossíntese
Fator VIII/genética
Camundongos
Proteínas Recombinantes
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (F8 protein, human); 0 (Recombinant Proteins); 9001-27-8 (Factor VIII)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160914
[St] Status:MEDLINE


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[PMID]:28185547
[Au] Autor:Pellin D; Di Serio C
[Ad] Endereço:University Center of Statistics for the Biomedical Sciences, Vita-Salute San Raffaele University, Via Olgettina 58, Milan, 20132, Italy. pellin.danilo@hsr.it.
[Ti] Título:A novel scan statistics approach for clustering identification and comparison in binary genomic data.
[So] Source:BMC Bioinformatics;17(Suppl 11):320, 2016 Sep 22.
[Is] ISSN:1471-2105
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: In biomedical research a relevant issue is to identify time intervals or portions of a n-dimensional support where a particular event of interest is more likely to occur than expected. Algorithms that require to specify a-priori number/dimension/length of clusters assumed for the data suffer from a high degree of arbitrariness whenever no precise information are available, and this may strongly affect final estimation on parameters. Within this framework, spatial scan-statistics have been proposed in the literature, representing a valid non-parametric alternative. RESULTS: We adapt the so called Bernoulli-model scan statistic to the genomic field and we propose a multivariate extension, named Relative Scan Statistics, for the comparison of two series of Bernoulli r.v. defined over a common support, with the final goal of highlighting unshared event rate variations. Using a probabilistic approach based on success probability estimates and comparison (likelihood based), we can exploit an hypothesis testing procedure to identify clusters and relative clusters. Both the univariate and the novel multivariate extension of the scan statistic confirm previously published findings. CONCLUSION: The method described in the paper represents a challenging application of scan statistics framework to problem related to genomic data. From a biological perspective, these tools offer the possibility to clinicians and researcher to improve their knowledge on viral vectors integrations process, allowing to focus their attention to restricted over-targeted portion of the genome.
[Mh] Termos MeSH primário: Algoritmos
Genômica/métodos
HIV/genética
Vírus da Leucemia Murina/genética
Proteínas Virais/genética
[Mh] Termos MeSH secundário: Análise por Conglomerados
Interpretação Estatística de Dados
Células-Tronco Hematopoéticas/citologia
Células-Tronco Hematopoéticas/metabolismo
Células-Tronco Hematopoéticas/virologia
Seres Humanos
Funções Verossimilhança
Integração Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Viral Proteins)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170211
[St] Status:MEDLINE
[do] DOI:10.1186/s12859-016-1173-8



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