Base de dados : MEDLINE
Pesquisa : G06.920 [Categoria DeCS]
Referências encontradas : 1260 [refinar]
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[PMID]:28961409
[Au] Autor:Williamson KE; Fuhrmann JJ; Wommack KE; Radosevich M
[Ad] Endereço:Biology Department, College of William and Mary, Williamsburg, Virginia 23185; email: kewilliamson@wm.edu.
[Ti] Título:Viruses in Soil Ecosystems: An Unknown Quantity Within an Unexplored Territory.
[So] Source:Annu Rev Virol;4(1):201-219, 2017 Sep 29.
[Is] ISSN:2327-0578
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Viral abundance in soils can range from below detection limits in hot deserts to over 1 billion per gram in wetlands. Abundance appears to be strongly influenced by water availability and temperature, but a lack of informational standards creates difficulties for cross-study analysis. Soil viral diversity is severely underestimated and undersampled, although current measures of viral richness are higher for soils than for aquatic ecosystems. Both morphometric and metagenomic analyses have raised questions about the prevalence of nontailed, ssDNA viruses in soils. Soil is complex and critically important to terrestrial biodiversity and human civilization, but impacts of viral activities on soil ecosystem services are poorly understood. While information from aquatic systems and medical microbiology suggests the potential for viral influences on nutrient cycles, food web interactions, gene transfer, and other key processes in soils, very few empirical data are available. To understand the soil virome, much work remains.
[Mh] Termos MeSH primário: Biodiversidade
Ecossistema
Microbiologia do Solo
Vírus/genética
[Mh] Termos MeSH secundário: DNA de Cadeia Simples/isolamento & purificação
Cadeia Alimentar
Transferência Genética Horizontal
Genoma Viral
Seres Humanos
Metagenômica
Fenômenos Fisiológicos Virais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (DNA, Single-Stranded)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170930
[St] Status:MEDLINE
[do] DOI:10.1146/annurev-virology-101416-041639


  2 / 1260 MEDLINE  
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[PMID]:28787582
[Au] Autor:Roossinck MJ; Bazán ER
[Ad] Endereço:Center for Infectious Disease Dynamics, Department of Plant Pathology and Environmental Microbiology, Pennsylvania State University, University Park, Pennsylvania 16802; email: mjr25@psu.edu.
[Ti] Título:Symbiosis: Viruses as Intimate Partners.
[So] Source:Annu Rev Virol;4(1):123-139, 2017 Sep 29.
[Is] ISSN:2327-0578
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Viruses must establish an intimate relationship with their hosts and vectors in order to infect, replicate, and disseminate; hence, viruses can be considered as symbionts with their hosts. Symbiotic relationships encompass different lifestyles, including antagonistic (or pathogenic, the most well-studied lifestyle for viruses), commensal (probably the most common lifestyle), and mutualistic (important beneficial partners). Symbiotic relationships can shape the evolution of the partners in a holobiont, and placing viruses in this context provides an important framework for understanding virus-host relationships and virus ecology. Although antagonistic relationships are thought to lead to coevolution, this is not always clear in virus-host interactions, and impacts on evolution may be complex. Commensalism implies a hitchhiking role for viruses-selfish elements just along for the ride. Mutualistic relationships have been described in detail in the past decade, and they reveal how important viruses are in considering host ecology. Ultimately, symbiosis can lead to symbiogenesis, or speciation through fusion, and the presence of large amounts of viral sequence in the genomes of everything from bacteria to humans, including some important functional genes, illustrates the significance of viral symbiogenesis in the evolution of all life on Earth.
[Mh] Termos MeSH primário: DNA Viral/genética
Interações Hospedeiro-Patógeno
Simbiose
Fenômenos Fisiológicos Virais
[Mh] Termos MeSH secundário: Animais
Bactérias/genética
Evolução Molecular
Genoma
Seres Humanos
Filogenia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (DNA, Viral)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170809
[St] Status:MEDLINE
[do] DOI:10.1146/annurev-virology-110615-042323


  3 / 1260 MEDLINE  
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[PMID]:28715974
[Au] Autor:Kaelber JT; Hryc CF; Chiu W
[Ad] Endereço:Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas 77030.
[Ti] Título:Electron Cryomicroscopy of Viruses at Near-Atomic Resolutions.
[So] Source:Annu Rev Virol;4(1):287-308, 2017 Sep 29.
[Is] ISSN:2327-0578
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recently, dozens of virus structures have been solved to resolutions between 2.5 and 5.0 Å by means of electron cryomicroscopy. With these structures we are now firmly within the "atomic age" of electron cryomicroscopy, as these studies can reveal atomic details of protein and nucleic acid topology and interactions between specific residues. This improvement in resolution has been the result of direct electron detectors and image processing advances. Although enforcing symmetry facilitates reaching near-atomic resolution with fewer particle images, it unfortunately obscures some biologically interesting components of a virus. New approaches on relaxing symmetry and exploring structure dynamics and heterogeneity of viral assemblies have revealed important insights into genome packaging, virion assembly, cell entry, and other stages of the viral life cycle. In the future, novel methods will be required to reveal yet-unknown structural conformations of viruses, relevant to their biological activities. Ultimately, these results hold the promise of answering many unresolved questions linking structural diversity of viruses to their biological functions.
[Mh] Termos MeSH primário: Microscopia Crioeletrônica
Processamento de Imagem Assistida por Computador/métodos
Vírion/ultraestrutura
Vírus/ultraestrutura
[Mh] Termos MeSH secundário: Cristalografia por Raios X
Genoma Viral
Modelos Moleculares
Ácidos Nucleicos/ultraestrutura
Conformação Proteica
Proteínas Virais/ultraestrutura
Vírion/fisiologia
Montagem de Vírus
Fenômenos Fisiológicos Virais
Vírus/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Nucleic Acids); 0 (Viral Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170719
[St] Status:MEDLINE
[do] DOI:10.1146/annurev-virology-101416-041921


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[PMID]:28615197
[Au] Autor:Naghavi MH; Walsh D
[Ad] Endereço:Department of Microbiology-Immunology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
[Ti] Título:Microtubule Regulation and Function during Virus Infection.
[So] Source:J Virol;91(16), 2017 Aug 15.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Microtubules (MTs) form a rapidly adaptable network of filaments that radiate throughout the cell. These dynamic arrays facilitate a wide range of cellular processes, including the capture, transport, and spatial organization of cargos and organelles, as well as changes in cell shape, polarity, and motility. Nucleating from MT-organizing centers, including but by no means limited to the centrosome, MTs undergo rapid transitions through phases of growth, pause, and catastrophe, continuously exploring and adapting to the intracellular environment. Subsets of MTs can become stabilized in response to environmental cues, acquiring distinguishing posttranslational modifications and performing discrete functions as specialized tracks for cargo trafficking. The dynamic behavior and organization of the MT array is regulated by MT-associated proteins (MAPs), which include a subset of highly specialized plus-end-tracking proteins (+TIPs) that respond to signaling cues to alter MT behavior. As pathogenic cargos, viruses require MTs to transport to and from their intracellular sites of replication. While interactions with and functions for MT motor proteins are well characterized and extensively reviewed for many viruses, this review focuses on MT filaments themselves. Changes in the spatial organization and dynamics of the MT array, mediated by virus- or host-induced changes to MT regulatory proteins, not only play a central role in the intracellular transport of virus particles but also regulate a wider range of processes critical to the outcome of infection.
[Mh] Termos MeSH primário: Interações Hospedeiro-Patógeno
Microtúbulos/metabolismo
Vírion/metabolismo
Fenômenos Fisiológicos Virais
[Mh] Termos MeSH secundário: Transporte Biológico
Regulação da Expressão Gênica
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170810
[Lr] Data última revisão:
170810
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170616
[St] Status:MEDLINE


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[PMID]:28588024
[Au] Autor:Keck KM; Moquin SA; He A; Fernandez SG; Somberg JJ; Liu SM; Martinez DM; Miranda JL
[Ad] Endereço:the Gladstone Institute of Virology and Immunology, San Francisco, California 94158.
[Ti] Título:Bromodomain and extraterminal inhibitors block the Epstein-Barr virus lytic cycle at two distinct steps.
[So] Source:J Biol Chem;292(32):13284-13295, 2017 Aug 11.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lytic infection by the Epstein-Barr virus (EBV) poses numerous health risks, such as infectious mononucleosis and lymphoproliferative disorder. Proteins in the bromodomain and extraterminal (BET) family regulate multiple stages of viral life cycles and provide promising intervention targets. Synthetic small molecules can bind to the bromodomains and disrupt function by preventing recognition of acetylated lysine substrates. We demonstrate that JQ1 and other BET inhibitors block two different steps in the sequential cascade of the EBV lytic cycle. BET inhibitors prevent expression of the viral immediate-early protein BZLF1. JQ1 alters transcription of genes controlled by the host protein BACH1, and BACH1 knockdown reduces BZLF1 expression. BET proteins also localize to the lytic origin of replication (OriLyt) genetic elements, and BET inhibitors prevent viral late gene expression. There JQ1 reduces BRD4 recruitment during reactivation to preclude replication initiation. This represents a rarely observed dual mode of action for drugs.
[Mh] Termos MeSH primário: Antivirais/farmacologia
Fatores de Transcrição de Zíper de Leucina Básica/antagonistas & inibidores
Proteínas de Grupos de Complementação da Anemia de Fanconi/antagonistas & inibidores
Regulação Viral da Expressão Gênica/efeitos dos fármacos
Herpesvirus Humano 4/efeitos dos fármacos
Proteínas Nucleares/antagonistas & inibidores
Transativadores/antagonistas & inibidores
Fatores de Transcrição/antagonistas & inibidores
Proteínas Virais/antagonistas & inibidores
[Mh] Termos MeSH secundário: Acetilação
Azepinas/farmacologia
Fatores de Transcrição de Zíper de Leucina Básica/química
Fatores de Transcrição de Zíper de Leucina Básica/genética
Fatores de Transcrição de Zíper de Leucina Básica/metabolismo
Linhagem Celular
Proteínas de Grupos de Complementação da Anemia de Fanconi/química
Proteínas de Grupos de Complementação da Anemia de Fanconi/genética
Proteínas de Grupos de Complementação da Anemia de Fanconi/metabolismo
Herpesvirus Humano 4/fisiologia
Interações Hospedeiro-Patógeno/efeitos dos fármacos
Seres Humanos
Lisina/metabolismo
Proteínas Nucleares/química
Proteínas Nucleares/genética
Proteínas Nucleares/metabolismo
Domínios e Motivos de Interação entre Proteínas
Processamento de Proteína Pós-Traducional
Transporte Proteico/efeitos dos fármacos
Interferência de RNA
Origem de Replicação/efeitos dos fármacos
Transativadores/química
Transativadores/genética
Transativadores/metabolismo
Fatores de Transcrição/química
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
Triazóis/farmacologia
Proteínas Virais/química
Proteínas Virais/genética
Proteínas Virais/metabolismo
Ativação Viral/efeitos dos fármacos
Fenômenos Fisiológicos Virais/efeitos dos fármacos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 ((+)-JQ1 compound); 0 (Antiviral Agents); 0 (Azepines); 0 (BACH1 protein, human); 0 (BRD4 protein, human); 0 (BZLF1 protein, Herpesvirus 4, Human); 0 (Basic-Leucine Zipper Transcription Factors); 0 (Fanconi Anemia Complementation Group Proteins); 0 (Nuclear Proteins); 0 (Trans-Activators); 0 (Transcription Factors); 0 (Triazoles); 0 (Viral Proteins); K3Z4F929H6 (Lysine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170825
[Lr] Data última revisão:
170825
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170608
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.751644


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[PMID]:28493815
[Au] Autor:Assetta B; Atwood WJ
[Ad] Endereço:.
[Ti] Título:The biology of JC polyomavirus.
[So] Source:Biol Chem;398(8):839-855, 2017 Jul 26.
[Is] ISSN:1437-4315
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:JC polyomavirus (JCPyV) is the causative agent of a fatal central nervous system demyelinating disease known as progressive multifocal leukoencephalopathy (PML). PML occurs in people with underlying immunodeficiency or in individuals being treated with potent immunomodulatory therapies. JCPyV is a DNA tumor virus with a double-stranded DNA genome and encodes a well-studied oncogene, large T antigen. Its host range is highly restricted to humans and only a few cell types support lytic infection in vivo or in vitro. Its oncogenic potential in humans has not been firmly established and the international committee on oncogenic viruses lists JCPyV as possibly carcinogenic. Significant progress has been made in understanding the biology of JCPyV and here we present an overview of the field and discuss some important questions that remain unanswered.
[Mh] Termos MeSH primário: Vírus JC
[Mh] Termos MeSH secundário: Animais
Genômica
Seres Humanos
Vírus JC/genética
Vírus JC/metabolismo
Vírus JC/fisiologia
Infecções por Polyomavirus
Transcrição Genética
Proteínas Virais/metabolismo
Fenômenos Fisiológicos Virais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Viral Proteins)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170731
[Lr] Data última revisão:
170731
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170512
[St] Status:MEDLINE


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[PMID]:28446620
[Au] Autor:Garbelli A; Riva V; Crespan E; Maga G
[Ad] Endereço:DNA Enzymology & Molecular Virology Unit, Institute of Molecular Genetics - CNR, via Abbiategrasso 207, Pavia 27100, Italy.
[Ti] Título:How to win the HIV-1 drug resistance hurdle race: running faster or jumping higher?
[So] Source:Biochem J;474(10):1559-1577, 2017 Apr 26.
[Is] ISSN:1470-8728
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Infections by the human immunodeficiency virus type 1 (HIV-1), the causative agent of the acquired immunodeficiency syndrome (AIDS), are still totaling an appalling 36.7 millions worldwide, with 1.1 million AIDS deaths/year and a similar number of yearly new infections. All this, in spite of the discovery of HIV-1 as the AIDS etiological agent more than 30 years ago and the introduction of an effective combinatorial antiretroviral therapy (cART), able to control disease progression, more than 20 years ago. Although very effective, current cART is plagued by the emergence of drug-resistant viral variants and most of the efforts in the development of novel direct-acting antiviral agents (DAAs) against HIV-1 have been devoted toward the fighting of resistance. In this review, rather than providing a detailed listing of all the drugs and the corresponding resistance mutations, we aim, through relevant examples, at presenting to the general reader the conceptual shift in the approaches that are being taken to overcome the viral resistance hurdle. From the classic 'running faster' strategy, based on the development of novel DAAs active against the mutant viruses selected by the previous drugs and/or presenting to the virus a high genetic barrier toward the development of resilience, to a 'jumping higher' approach, which looks at the cell, rather than the virus, as a source of valuable drug targets, in order to make the cellular environment non-permissive toward the replication of both wild-type and mutated viruses.
[Mh] Termos MeSH primário: Fármacos Anti-HIV/uso terapêutico
Desenho de Drogas
Farmacorresistência Viral Múltipla
Quimioterapia Combinada
Infecções por HIV/tratamento farmacológico
HIV-1/efeitos dos fármacos
Modelos Biológicos
[Mh] Termos MeSH secundário: Animais
Fármacos Anti-HIV/efeitos adversos
Fármacos Anti-HIV/química
Fármacos Anti-HIV/farmacologia
Terapia Antirretroviral de Alta Atividade/efeitos adversos
Antagonistas dos Receptores CCR5/química
Antagonistas dos Receptores CCR5/farmacologia
Antagonistas dos Receptores CCR5/uso terapêutico
RNA Helicases DEAD-box/antagonistas & inibidores
RNA Helicases DEAD-box/química
RNA Helicases DEAD-box/genética
RNA Helicases DEAD-box/metabolismo
Quimioterapia Combinada/efeitos adversos
Infecções por HIV/metabolismo
Infecções por HIV/virologia
Inibidores da Protease de HIV/efeitos adversos
Inibidores da Protease de HIV/química
Inibidores da Protease de HIV/farmacologia
Inibidores da Protease de HIV/uso terapêutico
HIV-1/genética
HIV-1/crescimento & desenvolvimento
HIV-1/fisiologia
Interações Hospedeiro-Patógeno/efeitos dos fármacos
Proteínas do Vírus da Imunodeficiência Humana/antagonistas & inibidores
Proteínas do Vírus da Imunodeficiência Humana/química
Proteínas do Vírus da Imunodeficiência Humana/genética
Proteínas do Vírus da Imunodeficiência Humana/metabolismo
Seres Humanos
Estrutura Molecular
Terapia de Alvo Molecular
Mutação
Conformação Proteica
Inibidores da Transcriptase Reversa/química
Inibidores da Transcriptase Reversa/farmacologia
Inibidores da Transcriptase Reversa/uso terapêutico
Fenômenos Fisiológicos Virais/efeitos dos fármacos
Replicação Viral/efeitos dos fármacos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-HIV Agents); 0 (CCR5 Receptor Antagonists); 0 (HIV Protease Inhibitors); 0 (Human Immunodeficiency Virus Proteins); 0 (Reverse Transcriptase Inhibitors); EC 3.6.1.- (DDX3X protein, human); EC 3.6.4.13 (DEAD-box RNA Helicases)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170623
[Lr] Data última revisão:
170623
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE
[do] DOI:10.1042/BCJ20160772


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[PMID]:28350815
[Au] Autor:Simon UK; Enzinger SM; Fink A
[Ad] Endereço:Center for Didactics of Biology, Karl-Franzens-University Graz, Schubertstraße, Graz, Austria.
[Ti] Título:"The evil virus cell": Students' knowledge and beliefs about viruses.
[So] Source:PLoS One;12(3):e0174402, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Education about virus biology at school is of pivotal interest to raise public awareness concerning means of disease transmission and, thus, methods to prevent infection, and to reduce unnecessary antibiotic treatment due to patient pressure on physicians in case of viral diseases such as influenza. This study aimed at making visible the knowledge of Austrian high school and university students with respect to virus biology, virus structure and health-education issues. The data presented here stem from comprehensive questionnaire analyses, including the task to draw a virus, from a cross-sectional study with 133 grade 7 and 199 grade 10 high school students, and 133 first-year biology and 181 first-year non-biology university students. Analyses were performed both quantitatively and qualitatively. ANOVA revealed a highly significant group effect for total knowledge relating to virus biology and health issues (F(3, 642) = 44.17, p < 0.01, η2p = 0.17). Specific post-hoc tests by means of the Tukey test showed significant differences between all groups (p < .01) with the exception of 1st year non-biology students and grade 10 high school students. Students enrolled in university-level biology outperformed all other groups, even though they had not yet encountered this topic at their courses; part of this phenomenon might be due to their affinity for learning about biological topics. However, even many first-year biology students had a high number of severe misconceptions, e.g., defining a virus as a pro- or eukaryotic cell, or falsely naming malaria as a viral disease. Since there was no significant difference in virus-related knowledge between high schools, virus biology seems to have been taught similarly among the tested schools. However, the majority of participants stated that the virus-related knowledge they had acquired at school was not sufficient. Based on the results presented here we urgently suggest improving and intensifying teaching this topic at school, since virus-related knowledge was by far too fragmentary among many participants. Such lack of health-relevant knowledge may contribute to pressure on physicians by patients to unnecessarily prescribe antibiotics, and possibly lead to potentially dangerous neglect concerning vaccination. The effectiveness of newly developed virus-related teaching units and material could be tested with the instrument used here.
[Mh] Termos MeSH primário: Educação em Saúde
Instituições Acadêmicas
Viroses/virologia
Fenômenos Fisiológicos Virais
[Mh] Termos MeSH secundário: Adolescente
Adulto
Análise de Variância
Antibacterianos/uso terapêutico
Áustria
Criança
Estudos Transversais
Feminino
Conhecimentos, Atitudes e Prática em Saúde
Seres Humanos
Masculino
Estudantes
Inquéritos e Questionários
Viroses/tratamento farmacológico
Viroses/transmissão
Vírus/química
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170329
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0174402


  9 / 1260 MEDLINE  
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[PMID]:28348067
[Au] Autor:Jean Beltran PM; Federspiel JD; Sheng X; Cristea IM
[Ad] Endereço:Department of Molecular Biology, Lewis Thomas Laboratory, Princeton University, Princeton, NJ, USA.
[Ti] Título:Proteomics and integrative omic approaches for understanding host-pathogen interactions and infectious diseases.
[So] Source:Mol Syst Biol;13(3):922, 2017 Mar 27.
[Is] ISSN:1744-4292
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Organisms are constantly exposed to microbial pathogens in their environments. When a pathogen meets its host, a series of intricate intracellular interactions shape the outcome of the infection. The understanding of these host-pathogen interactions is crucial for the development of treatments and preventive measures against infectious diseases. Over the past decade, proteomic approaches have become prime contributors to the discovery and understanding of host-pathogen interactions that represent anti- and pro-pathogenic cellular responses. Here, we review these proteomic methods and their application to studying viral and bacterial intracellular pathogens. We examine approaches for defining spatial and temporal host-pathogen protein interactions upon infection of a host cell. Further expanding the understanding of proteome organization during an infection, we discuss methods that characterize the regulation of host and pathogen proteomes through alterations in protein abundance, localization, and post-translational modifications. Finally, we highlight bioinformatic tools available for analyzing such proteomic datasets, as well as novel strategies for integrating proteomics with other omic tools, such as genomics, transcriptomics, and metabolomics, to obtain a systems-level understanding of infectious diseases.
[Mh] Termos MeSH primário: Doenças Transmissíveis/metabolismo
Biologia Computacional/métodos
Proteômica/métodos
[Mh] Termos MeSH secundário: Animais
Fenômenos Fisiológicos Bacterianos
Interações Hospedeiro-Patógeno
Seres Humanos
Metabolômica
Processamento de Proteína Pós-Traducional
Fenômenos Fisiológicos Virais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170923
[Lr] Data última revisão:
170923
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170329
[St] Status:MEDLINE
[do] DOI:10.15252/msb.20167062


  10 / 1260 MEDLINE  
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[PMID]:28207819
[Au] Autor:Hulo C; Masson P; de Castro E; Auchincloss AH; Foulger R; Poux S; Lomax J; Bougueleret L; Xenarios I; Le Mercier P
[Ad] Endereço:SIB Swiss Institute of Bioinformatics, CMU, University of Geneva Medical School, Geneva, Switzerland.
[Ti] Título:The ins and outs of eukaryotic viruses: Knowledge base and ontology of a viral infection.
[So] Source:PLoS One;12(2):e0171746, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Viruses are genetically diverse, infect a wide range of tissues and host cells and follow unique processes for replicating themselves. All these processes were investigated and indexed in ViralZone knowledge base. To facilitate standardizing data, a simple ontology of viral life-cycle terms was developed to provide a common vocabulary for annotating data sets. New terminology was developed to address unique viral replication cycle processes, and existing terminology was modified and adapted. The virus life-cycle is classically described by schematic pictures. Using this ontology, it can be represented by a combination of successive terms: "entry", "latency", "transcription", "replication" and "exit". Each of these parts is broken down into discrete steps. For example Zika virus "entry" is broken down in successive steps: "Attachment", "Apoptotic mimicry", "Viral endocytosis/ macropinocytosis", "Fusion with host endosomal membrane", "Viral factory". To demonstrate the utility of a standard ontology for virus biology, this work was completed by annotating virus data in the ViralZone, UniProtKB and Gene Ontology databases.
[Mh] Termos MeSH primário: Células Eucarióticas/virologia
Terminologia como Assunto
Viroses/virologia
Fenômenos Fisiológicos Virais
[Mh] Termos MeSH secundário: Bases de Dados Genéticas
Replicação Viral
Vírus/genética
Vírus/patogenicidade
[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:170217
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0171746



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