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  1 / 697 MEDLINE  
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[PMID]:28898711
[Au] Autor:Son KN; Liang Z; Lipton HL
[Ad] Endereço:Departments of Microbiology-Immunology, University of Illinois at Chicago, Chicago, IL, USA.
[Ti] Título:SJL bone marrow-derived macrophages do not have IRF3 mutations and are highly susceptible to Theiler's virus infection.
[So] Source:Virology;512:21-24, 2017 Dec.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:It is well known that SJL mice are susceptible to Theiler's murine encephalomyelitis virus (TMEV)-induced demyelinating disease while C57BL6 (B6) and B10 mice are resistant, and H-2 on a B10 background (B10.S) contributes modestly to susceptibility. A recent study linked two IRF3 non-conservative mutations in SJL compared to B10.S mice to resistance to TMEV infection of SJL peritoneal-derived macrophages, an observation of practical interest in light of the central role of IRF3 transcription factor in the type I interferon (IFN) response. However, we did not find these non-conservative mutations among SJL, B10.S, B6 and B10 mice in the IRF3 amino acid sequence, and show SJL bone marrow-derived macrophages infected with TMEV exhibit increased virus RNA replication and infectious virus yields as well as greater IL-6 production than C57Bl strain (including B10.S) cultures.
[Mh] Termos MeSH primário: Infecções por Cardiovirus/virologia
Predisposição Genética para Doença
Fator Regulador 3 de Interferon/metabolismo
Macrófagos/metabolismo
Theilovirus/fisiologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Regulação da Expressão Gênica/fisiologia
Fator Regulador 3 de Interferon/genética
Interleucina-6/genética
Interleucina-6/metabolismo
Camundongos
Camundongos Endogâmicos
Mutação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interferon Regulatory Factor-3); 0 (Interleukin-6); 0 (Irf3 protein, mouse)
[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:170913
[St] Status:MEDLINE


  2 / 697 MEDLINE  
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[PMID]:28675559
[Au] Autor:Barker-Haliski ML; Löscher W; White HS; Galanopoulou AS
[Ad] Endereço:Department of Pharmacy, School of Pharmacy, University of Washington, Seattle, Washington, U.S.A.
[Ti] Título:Neuroinflammation in epileptogenesis: Insights and translational perspectives from new models of epilepsy.
[So] Source:Epilepsia;58 Suppl 3:39-47, 2017 Jul.
[Is] ISSN:1528-1167
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Animal models have provided a wealth of information on mechanisms of epileptogenesis and comorbidogenesis, and have significantly advanced our ability to investigate the potential of new therapies. Processes implicating brain inflammation have been increasingly observed in epilepsy research. Herein we discuss the progress on animal models of epilepsy and comorbidities that inform us on the potential role of inflammation in epileptogenesis and comorbidity pathogenesis in rodent models of West syndrome and the Theiler's murine encephalomyelitis virus (TMEV) mouse model of viral encephalitis-induced epilepsy. Rat models of infantile spasms were generated in rat pups after right intracerebral injections of proinflammatory compounds (lipopolysaccharides with or without doxorubicin, or cytokines) and were longitudinally monitored for epileptic spasms and neurodevelopmental and cognitive deficits. Anti-inflammatory treatments were tested after the onset of spasms. The TMEV mouse model was induced with intracerebral administration of TMEV and prospective monitoring for handling-induced seizures or seizure susceptibility, as well as long-term evaluations of behavioral comorbidities of epilepsy. Inflammatory processes are evident in both models and are implicated in the pathogenesis of the observed seizures and comorbidities. A common feature of these models, based on the data so far available, is their pharmacoresistant profile. The presented data support the role of inflammatory pathways in epileptogenesis and comorbidities in two distinct epilepsy models. Pharmacoresistance is a common feature of both inflammation-based models. Utilization of these models may facilitate the identification of age-specific, syndrome- or etiology-specific therapies for the epilepsies and attendant comorbidities, including the drug-resistant forms.
[Mh] Termos MeSH primário: Infecções por Cardiovirus/imunologia
Modelos Animais de Doenças
Epilepsia/imunologia
Inflamação Neurogênica/tratamento farmacológico
Espasmos Infantis/tratamento farmacológico
Espasmos Infantis/imunologia
Theilovirus
Pesquisa Médica Translacional
[Mh] Termos MeSH secundário: Animais
Anticonvulsivantes/uso terapêutico
Descoberta de Drogas
Epilepsia Resistente a Medicamentos/tratamento farmacológico
Epilepsia Resistente a Medicamentos/imunologia
Epilepsia/tratamento farmacológico
Seres Humanos
Lactente
Mediadores da Inflamação/fisiologia
Camundongos
Inflamação Neurogênica/imunologia
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticonvulsants); 0 (Inflammation Mediators)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170705
[St] Status:MEDLINE
[do] DOI:10.1111/epi.13785


  3 / 697 MEDLINE  
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[PMID]:28445497
[Au] Autor:Kim SJ; Jin YH; Kim BS
[Ad] Endereço:Department of Microbiology-Immunology, Northwestern University Medical School, Chicago, Illinois.
[Ti] Título:Prostaglandin E2 produced following infection with Theiler's virus promotes the pathogenesis of demyelinating disease.
[So] Source:PLoS One;12(4):e0176406, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Infection of various cells with Theiler's murine encephalomyelitis virus (TMEV) activates the TLR- and melanoma differentiation-associated gene 5 (MDA5)-dependent pathways, resulting in the production of IL-1ß via the activation of caspase-1 upon assembly of the node-like receptor protein 3 (NLRP3) inflammasome. The role of IL-1ß in the pathogenesis of TMEV-induced demyelinating disease was previously investigated. However, the signaling effects of prostaglandin E2 (PGE2) downstream of the NLRP3 inflammasome on the immune responses to viral determinants and the pathogenesis of demyelinating disease are unknown. In this study, we investigated the levels of intermediate molecules leading to PGE2 signaling and the effects of blocking PGE2 signaling on the immune response to TMEV infection, viral persistence and the development of demyelinating disease. We demonstrate here that TMEV infection activates the NLRP3 inflammasome and PGE2 signaling much more vigorously in dendritic cells (DCs) and CD11b+ cells from susceptible SJL mice than in cells from resistant B6 mice. Inhibition of virus-induced PGE2 signaling using AH23848 resulted in decreased pathogenesis of demyelinating disease and viral loads in the central nervous system (CNS). In addition, AH23848 treatment caused the elevation of protective early IFN-γ-producing CD4+ and CD8+ T cell responses. Because the levels of IFN-ß were lower in AH23848-treated mice but the level of IL-6 was similar, over-production of pathogenic IFN-ß was modulated and the generation of IFN-γ-producing T cell responses was enhanced by the inhibition of PGE2 signaling. These results strongly suggest that excessive activation of the NLRP3 inflammasome and downstream PGE2 signaling contribute to the pathogenesis of TMEV-induced demyelinating disease.
[Mh] Termos MeSH primário: Infecções por Cardiovirus/complicações
Doenças Desmielinizantes/fisiopatologia
Dinoprostona/metabolismo
Theilovirus/fisiologia
[Mh] Termos MeSH secundário: Animais
Compostos de Bifenilo/farmacologia
Células da Medula Óssea/citologia
Encéfalo/metabolismo
Encéfalo/patologia
Linfócitos T CD4-Positivos/citologia
Linfócitos T CD4-Positivos/efeitos dos fármacos
Linfócitos T CD4-Positivos/metabolismo
Linfócitos T CD8-Positivos/citologia
Linfócitos T CD8-Positivos/efeitos dos fármacos
Linfócitos T CD8-Positivos/metabolismo
Infecções por Cardiovirus/fisiopatologia
Células Cultivadas
Doenças Desmielinizantes/virologia
Células Dendríticas/citologia
Células Dendríticas/imunologia
Células Dendríticas/metabolismo
Feminino
Expressão Gênica/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos C57BL
Neuroglia/citologia
Neuroglia/metabolismo
Receptores de Prostaglandina E Subtipo EP4/antagonistas & inibidores
Receptores de Prostaglandina E Subtipo EP4/metabolismo
Transdução de Sinais/efeitos dos fármacos
Medula Espinal/metabolismo
Medula Espinal/patologia
Carga Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biphenyl Compounds); 0 (Receptors, Prostaglandin E, EP4 Subtype); 81443-73-4 (AH 23848); K7Q1JQR04M (Dinoprostone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170427
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0176406


  4 / 697 MEDLINE  
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[PMID]:28237622
[Au] Autor:DePaula-Silva AB; Hanak TJ; Libbey JE; Fujinami RS
[Ad] Endereço:Department of Pathology, University of Utah School of Medicine, 15 North Medical Drive East, 2600 EEJMRB, Salt Lake City, UT 84112, USA.
[Ti] Título:Theiler's murine encephalomyelitis virus infection of SJL/J and C57BL/6J mice: Models for multiple sclerosis and epilepsy.
[So] Source:J Neuroimmunol;308:30-42, 2017 Jul 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Mouse models are great tools to study the mechanisms of disease development. Theiler's murine encephalomyelitis virus is used in two distinct viral infection mouse models to study the human diseases multiple sclerosis (MS) and epilepsy. Intracerebral (i.c.) infection of the SJL/J mouse strain results in persistent viral infection of the central nervous system and a MS-like disease, while i.c. infection of the C57BL/6J mouse strain results in acute seizures and epilepsy. Our understanding of how the immune system contributes to the development of two disparate diseases caused by the same virus is presented.
[Mh] Termos MeSH primário: Epilepsia
Esclerose Múltipla
Poliomielite/complicações
Theilovirus/patogenicidade
[Mh] Termos MeSH secundário: Imunidade Adaptativa
Animais
Antígenos CD/metabolismo
Linfócitos B/patologia
Linfócitos B/virologia
Modelos Animais de Doenças
Progressão da Doença
Epilepsia/genética
Epilepsia/imunologia
Epilepsia/patologia
Epilepsia/virologia
Macrófagos/patologia
Macrófagos/virologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Mutantes
Microglia/patologia
Microglia/virologia
Esclerose Múltipla/genética
Esclerose Múltipla/imunologia
Esclerose Múltipla/patologia
Esclerose Múltipla/virologia
Linfócitos T/patologia
Linfócitos T/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antigens, CD)
[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:170227
[St] Status:MEDLINE


  5 / 697 MEDLINE  
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[PMID]:28188174
[Au] Autor:Huseby Kelcher AM; Atanga PA; Gamez JD; Cumba Garcia LM; Teclaw SJ; Pavelko KD; Macura SI; Johnson AJ
[Ad] Endereço:Mayo Clinic Graduate School of Biomedical Sciences, Mayo Clinic, Rochester, Minnesota, USA.
[Ti] Título:Brain atrophy in picornavirus-infected FVB mice is dependent on the H-2D class I molecule.
[So] Source:FASEB J;31(6):2267-2275, 2017 Jun.
[Is] ISSN:1530-6860
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Brain atrophy is a common feature of numerous neurologic diseases in which the role of neuroinflammation remains ill-defined. In this study, we evaluated the contribution of major histocompatibility complex class I molecules to brain atrophy in Theiler's murine encephalomyelitis virus (TMEV)-infected transgenic FVB mice that express the D class I molecule. FVB/D and wild-type FVB mice were evaluated for changes in neuroinflammation, virus clearance, neuropathology, and development of brain atrophy T2-weighted MRI and subsequent 3-dimensional volumetric analysis. Significant brain atrophy and hippocampal neuronal loss were observed in TMEV-infected FVB/D mice, but not in wild-type FVB mice. Brain atrophy was observed at 1 mo postinfection and persisted through the 4-mo observation period. Of importance, virus-infected FVB/D mice elicited a strong CD8 T-cell response toward the immunodominant D -restricted TMEV-derived peptide, VP2 , and cleared TMEV from the CNS. In addition, immunofluorescence revealed CD8 T cells near virus-infected neurons; therefore, we hypothesize that class I restricted CD8 T-cell responses promote development of brain atrophy. This model provides an opportunity to analyze the contribution of immune cells to brain atrophy in a system where persistent virus infection and demyelination are not factors in long-term neuropathology.-Huseby Kelcher, A. M., Atanga, P. A., Gamez, J. D., Cumba Garcia, L. M., Teclaw, S. J., Pavelko, K. D., Macura, S. I., Johnson. A. J. Brain atrophy in picornavirus-infected FVB mice is dependent on the H-2D class I molecule.
[Mh] Termos MeSH primário: Encefalopatias/virologia
Encéfalo/patologia
Genes MHC Classe I/genética
Infecções por Picornaviridae/patologia
Theilovirus
[Mh] Termos MeSH secundário: Animais
Atrofia
Encéfalo/virologia
Linfócitos T CD8-Positivos/fisiologia
Modelos Animais de Doenças
Regulação da Expressão Gênica
Camundongos
Camundongos Endogâmicos
Camundongos Transgênicos
Neurônios/virologia
Infecções por Picornaviridae/imunologia
Carga Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170212
[St] Status:MEDLINE
[do] DOI:10.1096/fj.201601055R


  6 / 697 MEDLINE  
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[PMID]:27995661
[Au] Autor:Ramsay JD
[Ad] Endereço:Department of Veterinary Microbiology and Pathology, and Washington Animal Disease Diagnostic Laboratory, Washington State University, Pullman, Washington, USA.
[Ti] Título:Science-in-brief: Equine viral hepatitis.
[So] Source:Equine Vet J;49(2):138-140, 2017 Mar.
[Is] ISSN:2042-3306
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Infecções por Cardiovirus/veterinária
Infecções por Flaviviridae/veterinária
Hepatite C/veterinária
Hepatite Viral Animal/virologia
Doenças dos Cavalos/virologia
[Mh] Termos MeSH secundário: Animais
Flaviviridae
Infecções por Flaviviridae/virologia
Hepacivirus
Hepatite C/virologia
Cavalos
Theilovirus
[Pt] Tipo de publicação:EDITORIAL
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170703
[Lr] Data última revisão:
170703
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161221
[St] Status:MEDLINE
[do] DOI:10.1111/evj.12652


  7 / 697 MEDLINE  
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[PMID]:27723176
[Au] Autor:Tan SZ; Tan MZ; Prabakaran M
[Ad] Endereço:Temasek Life Science Laboratory, 1 Research Link, National University of Singapore, Singapore, Republic of Singapore.
[Ti] Título:Saffold virus, an emerging human cardiovirus.
[So] Source:Rev Med Virol;27(1), 2017 Jan.
[Is] ISSN:1099-1654
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Saffold virus (SAFV) is an emerging human cardiovirus that has been shown to be ubiquitous. Initial studies of SAFV focused on respiratory and gastrointestinal infection; however, it has also recently been associated with diverse clinical symptoms including the endocrine, cardiovascular, and neurological systems. Given the systemic nature of SAFV, and its high prevalence, understanding its pathogenicity and clinical impact is of utmost importance. This comprehensive review highlights and discusses recent developments in epidemiology, human pathogenicity, animal, and molecular studies related to SAFV. It also provides detailed insights into the neuropathogenicity of SAFV. We argue that human studies have been confounded by coinfections and therefore require support from robust molecular and animal research. Thereby, we aim to provide foresight into further research to better understand this emerging virus.
[Mh] Termos MeSH primário: Infecções por Cardiovirus/epidemiologia
Infecções por Cardiovirus/virologia
Doenças Transmissíveis Emergentes/epidemiologia
Doenças Transmissíveis Emergentes/virologia
Theilovirus/isolamento & purificação
[Mh] Termos MeSH secundário: Animais
Infecções por Cardiovirus/patologia
Doenças Transmissíveis Emergentes/patologia
Modelos Animais de Doenças
Seres Humanos
Prevalência
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161011
[St] Status:MEDLINE
[do] DOI:10.1002/rmv.1908


  8 / 697 MEDLINE  
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[PMID]:27911409
[Au] Autor:Gilli F; Royce DB; Pachner AR
[Ad] Endereço:Department of Neurology, Geisel School of Medicine at Dartmouth; Francesca.Gilli@dartmouth.edu.
[Ti] Título:Measuring Progressive Neurological Disability in a Mouse Model of Multiple Sclerosis.
[So] Source:J Vis Exp;(117), 2016 Nov 14.
[Is] ISSN:1940-087X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:After intracerebral infection with the Theiler's Murine Encephalomyelitis Virus (TMEV), susceptible SJL mice develop a chronic-progressive demyelinating disease, with clinical features similar to the progressive forms of multiple sclerosis (MS). The mice show progressive disability with loss of motor and sensory functions, which can be assessed with multiple apparatuses and protocols. Among them, the Rotarod performance test is a very common behavioral test, its advantage being that it provides objective measurements, but it is often used assuming that it is straightforward and simple. In contrast to visual scoring systems used in some models of MS, which are highly subjective, the Rotarod test generates an objective, measurable, continuous variable (i.e., length of time), allowing almost perfect inter-rater concordances. However, inter-laboratory reliability is only achieved if the various testing parameters are replicated. In this manuscript, recommendations of specific testing parameters, such as size, speed, and acceleration of the rod; amount of training given to the animals; and data processing, are presented for the Rotarod test.
[Mh] Termos MeSH primário: Esclerose Múltipla
[Mh] Termos MeSH secundário: Animais
Infecções por Cardiovirus/complicações
Doenças Desmielinizantes/etiologia
Doenças Desmielinizantes/fisiopatologia
Modelos Animais de Doenças
Progressão da Doença
Camundongos
Camundongos Endogâmicos
Esclerose Múltipla/fisiopatologia
Theilovirus
[Pt] Tipo de publicação:JOURNAL ARTICLE; VIDEO-AUDIO MEDIA
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161203
[St] Status:MEDLINE
[do] DOI:10.3791/54616


  9 / 697 MEDLINE  
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[PMID]:27887630
[Au] Autor:Tan SZ; Prabakaran M
[Ad] Endereço:Temasek Life Science Laboratory, 1 Research Link, National University of Singapore, Singapore, 117604, Republic of Singapore.
[Ti] Título:Immunohistochemical insights into Saffold virus infection of the brain of juvenile AG129 mice.
[So] Source:Virol J;13(1):191, 2016 Nov 25.
[Is] ISSN:1743-422X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Saffold Virus (SAFV) is a human cardiovirus that is suspected of causing infection of the central nervous system (CNS) in children. While recent animal studies have started to elucidate the pathogenesis of SAFV, very little is known about the mechanisms behind it. METHOD: In this study, we attempted to elucidate some of the mechanisms of the pathogenesis of SAFV in the brain of a juvenile mouse model by using immunohistochemical methods. RESULTS: We first showed that SAFV is able to infect both neuronal and glial cells in the brain of 2 week-old AG129 mice. We then showed that SAFV is able to induce apoptosis in both neuronal and glial cells in the brain. Lastly, we showed that SAFV infection does not show any signs of gross demyelination in the brain. CONCLUSION: Overall, our results provide important insights into the mechanisms of SAFV in the brain.
[Mh] Termos MeSH primário: Encéfalo/patologia
Encéfalo/virologia
Infecções por Cardiovirus/patologia
Infecções por Cardiovirus/virologia
Encefalite Viral/patologia
Encefalite Viral/virologia
Theilovirus/isolamento & purificação
[Mh] Termos MeSH secundário: Animais
Apoptose
Modelos Animais de Doenças
Imuno-Histoquímica
Camundongos
Neuroglia/virologia
Neurônios/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161127
[St] Status:MEDLINE


  10 / 697 MEDLINE  
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[PMID]:27855706
[Au] Autor:Wootla B; Denic A; Watzlawik JO; Warrington AE; Zoecklein LJ; Papke-Norton LM; David C; Rodriguez M
[Ad] Endereço:Department of Neurology, Mayo Clinic, 200 First Street SW, Rochester, MN, 55905, USA.
[Ti] Título:Human class I major histocompatibility complex alleles determine central nervous system injury versus repair.
[So] Source:J Neuroinflammation;13(1):293, 2016 Nov 17.
[Is] ISSN:1742-2094
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: We investigated the role of human HLA class I molecules in persistent central nervous system (CNS) injury versus repair following virus infection of the CNS. METHODS: Human class I A11 and B27 transgenic human beta-2 microglobulin positive (Hß2m ) mice of the H-2 background were generated on a combined class I-deficient (mouse beta-2 microglobulin deficient, ß2m ) and class II-deficient (mouse Aß ) phenotype. Intracranial infection with Theiler's murine encephalomyelitis virus (TMEV) in susceptible SJL mice results in acute encephalitis with prominent injury in the hippocampus, striatum, and cortex. RESULTS: Following infection with TMEV, a picornavirus, the Aß .ß2m mice lacking active immune responses died within 18 to 21 days post-infection. These mice showed severe encephalomyelitis due to rapid replication of the viral genome. In contrast, transgenic Hß2m mice with insertion of a single human class I MHC gene in the absence of human or mouse class II survived the acute infection. Both A11 and B27 mice significantly controlled virus RNA expression by 45 days and did not develop late-onset spinal cord demyelination. By 45 days post-infection (DPI), B27 transgenic mice showed almost complete repair of the virus-induced brain injury, but A11 mice conversely showed persistent severe hippocampal and cortical injury. CONCLUSIONS: The findings support the hypothesis that the expression of a single human class I MHC molecule, independent of persistent virus infection, influences the extent of sub frequent chronic neuronal injury or repair in the absence of a class II MHC immune response.
[Mh] Termos MeSH primário: Infecções por Cardiovirus/patologia
Sistema Nervoso Central/patologia
Sistema Nervoso Central/virologia
Antígenos de Histocompatibilidade Classe I/metabolismo
Theilovirus/fisiologia
[Mh] Termos MeSH secundário: Análise de Variância
Animais
Anticorpos/metabolismo
Modelos Animais de Doenças
Citometria de Fluxo
Antígeno HLA-A11/metabolismo
Antígeno HLA-B27/metabolismo
Antígenos de Histocompatibilidade Classe I/genética
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
RNA Mensageiro
Proteínas Virais/genética
Proteínas Virais/imunologia
Proteínas Virais/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (HLA-A11 Antigen); 0 (HLA-B27 Antigen); 0 (Histocompatibility Antigens Class I); 0 (RNA, Messenger); 0 (Viral Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161119
[St] Status:MEDLINE



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BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde