Bibliografias temáticas / Neurovirulence

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Literatura científica selecionada sobre o tema "Neurovirulence"

Autor: Grafiati

Publicado: 4 de junho de 2021

Última modificação: 4 de fevereiro de 2022

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Artigos de revistas sobre o assunto "Neurovirulence"

Rubin, Steven A., Georgios Amexis, Mikhail Pletnikov, Jacqueline Vanderzanden, Jeremy Mauldin, Christian Sauder, Tahir Malik, Konstantin Chumakov e Kathryn M. Carbone. "Changes in Mumps Virus Gene Sequence Associated with Variability in Neurovirulent Phenotype". Journal of Virology 77, n.º 21 (1 de novembro de 2003): 11616–24. http://dx.doi.org/10.1128/jvi.77.21.11616-11624.2003.

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ABSTRACT Mumps virus is highly neurotropic and, prior to widespread vaccination programs, was the major cause of viral meningitis in the United States. Nonetheless, the genetic basis of mumps virus neurotropism and neurovirulence was until recently not understood, largely due to the lack of an animal model. Here, nonneurovirulent (Jeryl Lynn vaccine) and highly neurovirulent (88-1961 wild type) mumps virus strains were passaged in human neural cells or in chicken fibroblast cells with the goal of neuroadapting or neuroattenuating the viruses, respectively. When tested in our rat neurovirulence assay against the respective parental strains, a Jeryl Lynn virus variant with an enhanced propensity for replication (neurotropism) and damage (neurovirulence) in the brain and an 88-1961 wild-type virus variant with decreased neurotropic and neurovirulent properties were recovered. To determine the molecular basis for the observed differences in neurovirulence and neuroattenuation, the complete genomes of the parental strains and their variants were fully sequenced. A comparison at the nucleotide level associated three amino acid changes with enhanced neurovirulence of the neuroadapted vaccine strain: one each in the nucleoprotein, matrix protein, and polymerase and three amino acid changes with reduced neurovirulence of the neuroattenuated wild-type strain: one each in the fusion protein, hemagglutinin-neuraminidase protein, and polymerase. The potential role of these amino acid changes in neurotropism, neurovirulence, and neuroattenuation is discussed.

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Rubin, Steven A., Mikhail Pletnikov e Kathryn M. Carbone. "Comparison of the Neurovirulence of a Vaccine and a Wild-Type Mumps Virus Strain in the Developing Rat Brain". Journal of Virology 72, n.º 10 (1 de outubro de 1998): 8037–42. http://dx.doi.org/10.1128/jvi.72.10.8037-8042.1998.

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ABSTRACT Prior to the adoption of widespread vaccination programs, mumps virus was the leading cause of virus-induced central nervous system (CNS) disease. Mumps virus-associated CNS complications in vaccinees continue to be reported; outside the United States, some of these complications have been attributed to vaccination with insufficiently attenuated neurovirulent vaccine strains. The development of potentially neurovirulent, live, attenuated mumps virus vaccines stems largely from the lack of an animal model that can reliably predict the neurovirulence of mumps virus vaccine candidates in humans. The lack of an effective safety test with which to measure mumps virus neurovirulence has also hindered analysis of the neuropathogenesis of mumps virus infection and the identification of molecular determinants of neurovirulence. In this report we show, for the first time, that mumps virus infection of the neonatal rat leads to developmental abnormalities in the cerebellum due to cerebellar granule cell migration defects. The incidence of the cerebellar abnormalities and other neuropathological and clinical outcomes of mumps virus infection of the neonatal rat brain demonstrated the ability of this model to distinguish neurovirulent (Kilham) from nonneurovirulent (Jeryl Lynn) mumps virus strains. Thus, this neonatal rat model may prove useful in evaluating the neurovirulence potential of new live, attenuated vaccine strains and may also be of value in elucidating the molecular basis of mumps virus neurovirulence.

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Li, Yun, Li Fu, Donna M. Gonzales e Ehud Lavi. "Coronavirus Neurovirulence Correlates with the Ability of the Virus To Induce Proinflammatory Cytokine Signals from Astrocytes and Microglia". Journal of Virology 78, n.º 7 (1 de abril de 2004): 3398–406. http://dx.doi.org/10.1128/jvi.78.7.3398-3406.2004.

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ABSTRACT The molecular and cellular basis of coronavirus neurovirulence is poorly understood. Since neurovirulence may be determined at the early stages of infection of the central nervous system (CNS), we hypothesize that it may depend on the ability of the virus to induce proinflammatory signals from brain cells for the recruitment of blood-derived inflammatory cells. To test this hypothesis, we studied the interaction between coronaviruses (mouse hepatitis virus) of different neurovirulences with primary cell cultures of brain immune cells (astrocytes and microglia) and mouse tissues. We found that the level of neurovirulence of the virus correlates with its differential ability to induce proinflammatory cytokines (interleukin 12 [IL-12] p40, tumor necrosis factor alpha, IL-6, IL-15, and IL-1β) in astrocytes and microglia and in mouse brains and spinal cords. These findings suggest that coronavirus neurovirulence may depend on a novel discriminatory ability of astrocytes and microglia to induce a proinflammatory response in the CNS.

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Goldsmith, Kim, Wei Chen, David C. Johnson e Robert L. Hendricks. "Infected Cell Protein (ICP)47 Enhances Herpes Simplex Virus Neurovirulence by Blocking the CD8+ T Cell Response". Journal of Experimental Medicine 187, n.º 3 (2 de fevereiro de 1998): 341–48. http://dx.doi.org/10.1084/jem.187.3.341.

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The herpes simplex virus (HSV) infected cell protein (ICP)47 blocks CD8+ T cell recognition of infected cells by inhibiting the transporter associated with antigen presentation (TAP). In vivo, HSV-1 replicates in two distinct tissues: in epithelial mucosa or epidermis, where the virus enters sensory neurons; and in the peripheral and central nervous system, where acute and subsequently latent infections occur. Here, we show that an HSV-1 ICP47− mutant is less neurovirulent than wild-type HSV-1 in mice, but replicates normally in epithelial tissues. The reduced neurovirulence of the ICP47− mutant was due to a protective CD8+ T cell response. When compared with wild-type virus, the ICP47− mutant expressed reduced neurovirulence in immunologically normal mice, and T cell–deficient nude mice after reconstitution with CD8+ T cells. However, the ICP47− mutant exhibited normal neurovirulence in mice that were acutely depleted of CD8+ T cells, and in nude mice that were not reconstituted, or were reconstituted with CD4+ T cells. In contrast, CD8+ T cell depletion did not increase the neurovirulence of an unrelated, attenuated HSV-1 glycoprotein (g)E− mutant. ICP47 is the first viral protein shown to influence neurovirulence by inhibiting CD8+ T cell protection.

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Moeller, Kerstin, Iain Duffy, Paul Duprex, Bert Rima, Rudi Beschorner, Susanne Fauser, Richard Meyermann, Stefan Niewiesk, Volker ter Meulen e Jürgen Schneider-Schaulies. "Recombinant Measles Viruses Expressing Altered Hemagglutinin (H) Genes: Functional Separation of Mutations Determining H Antibody Escape from Neurovirulence". Journal of Virology 75, n.º 16 (15 de agosto de 2001): 7612–20. http://dx.doi.org/10.1128/jvi.75.16.7612-7620.2001.

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ABSTRACT Measles virus (MV) strain CAM/RB, which was adapted to growth in the brain of newborn rodents, is highly neurovirulent. It has been reported earlier that experimentally selected virus variants escaping from the monoclonal antibodies (MAbs) Nc32 and L77 to hemagglutinin (H) preserved their neurovirulence, whereas mutants escaping MAbs K71 and K29 were found to be strongly attenuated (U. G. Liebert et al., J. Virol. 68:1486–1493, 1994). To investigate the molecular basis of these findings, we have generated a panel of recombinant MVs expressing the H protein from CAM/RB and introduced the amino acid substitutions thought to be responsible for antibody escape and/or neurovirulence. Using these recombinant viruses, we identified the amino acid changes conferring escape from the MAbs L77 (377R→Q and 378M→K), Nc32 (388G→S), K71 (492E→K and 550S→P), and K29 (535E→G). When the corresponding recombinant viruses were tested in brains of newborn rodents, we found that the mutations mediating antibody escape did not confer differential neurovirulence. In contrast, however, replacement of two different amino acids, at positions 195G→R and 200S→N, which had been described for the escape mutant set, caused the change in neurovirulence. Thus, antibody escape and neurovirulence appear not to be associated with the same structural alterations of the MV H protein.

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Bray, Michael, Ruhe Men, Issei Tokimatsu e Ching-Juh Lai. "Genetic Determinants Responsible for Acquisition of Dengue Type 2 Virus Mouse Neurovirulence". Journal of Virology 72, n.º 2 (1 de fevereiro de 1998): 1647–51. http://dx.doi.org/10.1128/jvi.72.2.1647-1651.1998.

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ABSTRACT Studies conducted some 50 years ago showed that serial intracerebral passage of dengue viruses in mice selected for neurovirulent mutants that also exhibited significant attenuation for humans. We investigated the genetic basis of mouse neurovirulence of dengue virus because it might be directly or indirectly associated with attenuation for humans. Analysis of the sequence in the C-PreM-E-NS1 region of the parental dengue type 2 virus (DEN2) New Guinea C (NGC) strain and its mouse-adapted, neurovirulent mutant revealed that 10 nucleotide changes occurred during serial passage in mice. Seven of these changes resulted in amino acid substitutions, i.e., Leu55-Phe and Arg57-Lys in PreM, Glu71-Asp, Glu126-Lys, Phe402-Ile, and Thr454-Ile in E, and Arg105-Gln in NS1. The sequence of C was fully conserved between the parental and mutant DEN2. We constructed intertypic chimeric dengue viruses that contained the PreM-E genes or only the NS1 gene of neurovirulent DEN2 NGC substituting for the corresponding genes of DEN4. The DEN2 (PreM-E)/DEN4 chimera was neurovirulent for mice, whereas DEN2 (NS1)/DEN4 was not. The mutations present in the neurovirulent DEN2 PreM-E genes were then substituted singly or in combination into the sequence of the nonneurovirulent, parental DEN2. Intracerebral titration of the various mutant chimeras so produced identified two amino acid changes, namely, Glu71-Asp and Glu126-Lys, in DEN2 E as being responsible for mouse neurovirulence. The conservative amino acid change of Glu71-Asp probably had a minor effect, if any. The Glu126-Lys substitution in DEN2 E, representing a change from a negatively charged amino acid to a positively charged amino acid, most likely plays an important role in conferring mouse neurovirulence.

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Perng, Guey-Chuen, Kevin R. Mott, Nelson Osorio, Ada Yukht, Susan Salina, Quynh-Hoa Nguyen, Anthony B. Nesburn e Steven L. Wechsler. "Herpes simplex virus type 1 mutants containing the KOS strain ICP34.5 gene in place of the McKrae ICP34.5 gene have McKrae-like spontaneous reactivation but non-McKrae-like virulence". Journal of General Virology 83, n.º 12 (1 de dezembro de 2002): 2933–42. http://dx.doi.org/10.1099/0022-1317-83-12-2933.

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Herpes simplex virus type 1 (HSV-1) strain McKrae is neurovirulent in rabbits infected by the ocular route, causing fatal encephalitis in approximately 50% of the animals, and has a high-level spontaneous reactivation phenotype, with 10% of rabbit eyes containing reactivated virus at any given time. In contrast, HSV-1 strain KOS is completely avirulent (no rabbits die) and has a completely negative spontaneous reactivation phenotype. Mutations of the ICP34.5 gene can reduce the neurovirulence of HSV-1 strains McKrae and 17syn+ by up to 100000-fold. ICP34.5 mutants also have reduced spontaneous reactivation phenotypes. To determine whether differences in the ICP34.5 gene might be involved in the reduced neurovirulence and spontaneous reactivation phenotypes of KOS compared with McKrae, we constructed chimeric viruses containing the KOS ICP34.5 gene in place of the McKrae ICP34.5 gene. Rabbits ocularly infected with the chimeric viruses had a high spontaneous reactivation phenotype indistinguishable from McKrae. In contrast, neurovirulence of the chimeric viruses was decreased compared with McKrae. Thus, one or more ‘defects’ in the KOS ICP34.5 gene appeared to be at least partially responsible for the reduced neurovirulence of KOS compared with McKrae. However, there appeared to be no ‘defect′ in the KOS ICP34.5 function required for efficient spontaneous reactivation.

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Iacono, Kathryn T., Lubna Kazi e Susan R. Weiss. "Both Spike and Background Genes Contribute to Murine Coronavirus Neurovirulence". Journal of Virology 80, n.º 14 (15 de julho de 2006): 6834–43. http://dx.doi.org/10.1128/jvi.00432-06.

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ABSTRACT Various strains of mouse hepatitis virus (MHV) exhibit different pathogenic phenotypes. Infection with the A59 strain of MHV induces both encephalitis and hepatitis, while the highly neurovirulent JHM strain induces a fatal encephalitis with little, if any, hepatitis. The pathogenic phenotype for each strain is determined by the genetic composition of the viral genome, as well as the host immune response. Using isogenic recombinant viruses with A59 background genes differing only in the spike gene, we have previously shown that high neurovirulence is associated with the JHM spike protein, the protein responsible for attachment to the host cell receptor (J. J. Phillips, M. M. Chua, G. F. Rall, and S. R. Weiss, Virology 301:109-120, 2002). Using another set of isogenic recombinant viruses with JHM background genes expressing either the JHM or A59 spike, we have further investigated the roles of viral genes in pathogenesis. Here, we demonstrate that the high neurovirulence of JHM is associated with accelerated spread through the brain and a heightened innate immune response that is characterized by high numbers of infiltrating neutrophils and macrophages, suggesting an immunopathogenic component to neurovirulence. While expression of the JHM spike is sufficient to confer a neurovirulent phenotype, as well as increased macrophage infiltration, background genes contribute to virulence as well, at least in part, by dictating the extent of the T-cell immune response.

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Portis, J. L., P. Askovich, J. Austin, Y. Gutierrez-Cotto e F. J. McAtee. "The Degree of Folding Instability of the Envelope Protein of a Neurovirulent Murine Retrovirus Correlates with the Severity of the Neurological Disease". Journal of Virology 83, n.º 12 (1 de abril de 2009): 6079–86. http://dx.doi.org/10.1128/jvi.02647-08.

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ABSTRACT A small group of ecotropic murine retroviruses cause a spongiform neurodegenerative disease manifested by tremor, paralysis, and wasting. The neurovirulence of these viruses has long been known to be determined by the sequence of the viral envelope protein, although the nature of the neurotoxicity remains to be clarified. Studies on the neurovirulent viruses FrCasNC and Moloney murine leukemia virus ts1 indicate that the nascent envelope protein misfolds, is retained in the endoplasmic reticulum (ER), and induces an unfolded protein response. In the present study we constructed a series of viruses with chimeric envelope genes containing segments from virulent and avirulent retroviruses. Each of the viruses studied was highly neuroinvasive but differed in the severity of the neurological disease they induced. Only viruses that contained the receptor-binding domain (RBD) of the neurovirulent virus induced neurological disease. Likewise, only viruses containing the RBD of the neurovirulent virus exhibited increased binding of the ER chaperone BiP to the envelope precursor protein and induced the unfolded protein response. Thus, the RBD determined both neurovirulence and folding instability. Among viruses carrying the neurovirulent RBD, the severity of the disease was increased when envelope sequences from the neurovirulent virus outside the RBD were also present. Interestingly, these sequences appeared to further increase the degree of folding instability (BiP binding) of the viral envelope protein. These results provide strong support for the hypothesis that this spongiform neurodegenerative disease represents a virus-induced protein folding disorder.

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Arroyo, Juan, Farshad Guirakhoo, Sabine Fenner, Zhen-Xi Zhang, Thomas P. Monath e Thomas J. Chambers. "Molecular Basis for Attenuation of Neurovirulence of a Yellow Fever Virus/Japanese Encephalitis Virus Chimera Vaccine (ChimeriVax-JE)". Journal of Virology 75, n.º 2 (15 de janeiro de 2001): 934–42. http://dx.doi.org/10.1128/jvi.75.2.934-942.2001.

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ABSTRACT A yellow fever virus (YFV)/Japanese encephalitis virus (JEV) chimera in which the structural proteins prM and E of YFV 17D are replaced with those of the JEV SA14-14-2 vaccine strain is under evaluation as a candidate vaccine against Japanese encephalitis. The chimera (YFV/JEV SA14-14-2, or ChimeriVax-JE) is less neurovirulent than is YFV 17D vaccine in mouse and nonhuman primate models (F. Guirakhoo et al., Virology 257:363–372, 1999; T. P. Monath et al., Vaccine 17:1869–1882, 1999). Attenuation depends on the presence of the JEV SA14-14-2 E protein, as shown by the high neurovirulence of an analogous YFV/JEV Nakayama chimera derived from the wild JEV Nakayama strain (T. J. Chambers, A. Nestorowicz, P. W. Mason, and C. M. Rice, J. Virol. 73:3095–3101, 1999). Ten amino acid differences exist between the E proteins of ChimeriVax-JE and the YFV/JEV Nakayama virus, four of which are predicted to be neurovirulence determinants based on various sequence comparisons. To identify residues that are involved in attenuation, a series of intratypic YFV/JEV chimeras containing either single or multiple amino acid substitutions were engineered and tested for mouse neurovirulence. Reversions in at least three distinct clusters were required to restore the neurovirulence typical of the YFV/JEV Nakayama virus. Different combinations of cluster-specific reversions could confer neurovirulence; however, residue 138 of the E protein (E138) exhibited a dominant effect. No single amino acid reversion produced a phenotype significantly different from that of the ChimeriVax-JE parent. Together with the known genetic stability of the virus during prolonged cell culture and mouse brain passage, these findings support the candidacy of this experimental vaccine as a novel live-attenuated viral vaccine against Japanese encephalitis.

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Teses / dissertações sobre o assunto "Neurovirulence"

Lemon, Ken. "Molecular determinants of mumps virus neurovirulence". Thesis, Queen's University Belfast, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.426705.

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Dambrosi, Sarah. "Neurovirulence et latence des virus Herpes simplex mutants". Thesis, Université Laval, 2009. http://www.theses.ulaval.ca/2009/26368/26368.pdf.

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Tecle, Tesfaldet. "Biomolecular characterization of mumps virus genotypes with varying neurovirulence /". Stockholm : [Karolinska institutets bibl.], 2002. http://diss.kib.ki.se/2002/91-7349-234-5.

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Sutherland, Danica Marie. "Functions of the Viral Attachment Protein in Reovirus Neurovirulence". Thesis, Vanderbilt University, 2019. http://pqdtopen.proquest.com/#viewpdf?dispub=13877290.

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Viral invasion of the central nervous system (CNS) is a significant cause of morbidity and mortlity worldwide, particularly in young children (1). The nervous system presents a challenging site for viruses to access, with multiple physical and immunological barriers that limit pathogen invasion. To invade the CNS, viruses must access cell-surface receptors for binding and entry events. Virus-receptor interactions also govern tropism and often control disease type and severity. For many viruses, the identities of receptors and other cellular determinants of viral tropism remain elusive. Understanding where and how viral capsid components engage neural receptors and the effect of these interactions on tropism and disease may illuminate targets to prevent viral neuroinvasion.

Mammalian orthoreoviruses (reoviruses) provide a highly tractable and well-established system to identify mechanisms of viral entry into the CNS. Reoviruses are non-enveloped particles containing a 10-segmented, double-stranded (ds) RNA genome that replicate well in culture and can be altered via a robust reverse-genetics system (2, 3). While reovirus causes similar age-restricted disease in many young mammals (4-6), most studies employ newborn mice. Following peroral or intracranial inoculation of newborn mice, reovirus displays serotype-specific patterns of tropism in the brain and concomitant disease (Fig. I-1). Serotype 1 (T1) strains infect ependymal cells lining the ventricles of the brain and cause a non-lethal hydrocephalus (7). In contrast, serotype 3 (T3) strains infect specific neuron populations in the CNS and produce a fulminant, and often lethal, encephalitis (8). These differences in tropism and disease have been genetically mapped to the reovirus S1 gene using single-gene reassortant viruses (9). However, viral and host gene sequences that mediate either T1 or T3 tropism have not been defined.

In Chapter I of my dissertation, I introduce key themes about mechanisms of neuroinvasion and the disease consequences of CNS infection. I describe fundamental knowledge and open areas of research pertaining to reovirus infection in the CNS and expand on reovirus-receptor interactions. I conclude Chapter I with a summary of viral oncolytic therapies and highlight strengths and opportunities for improvement of reovirus oncolytics. In Chapter II, I describe the design and implementation of σ1- chimeric reoviruses to identify sequences in the S1 gene that dictate neurotropism and virulence in the CNS. In these studies, I found that homologous sequences at the viriondistal end of the viral attachment protein are responsible for neuron and ependymal cell targeting. In Chapter III, I identify sequences of the NgR1 reovirus receptor that are required for binding and post-binding functions and elucidate the viral ligand for NgR1, which is the σ3 outer-capsid protein, using a combination of genetic, biochemical, and structural approaches. Finally, in Chapter IV, I review conclusions from results presented in Chapters II and III, examine new questions raised by these studies, and discuss future directions of this work. Collectively, my dissertation research has unveiled viral and host sequences that contribute to neural cell targeting and will improve strategies and knowledge to design targeted oncolytic therapies.

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Renszel, Krystal Marie. "USING MUTAGENESIS AND STEM CELLS TO UNDERSTAND RETROVIRAL NEUROVIRULENCE". Kent State University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=kent1254659655.

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Fraipont, Florence de. "Caractérisation et utilisation des déterminants phénotypiques et moléculaires de la neurovirulence et de l'atténuation des souches de poliovirus". Strasbourg 1, 1992. http://www.theses.fr/1992STR15085.

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CHRISTODOULOU, CHRISTINA. "Le neurotropisme du poliovirus : bases moleculaires de la neurovirulence, et persistance virale". Paris 7, 1990. http://www.theses.fr/1990PA077022.

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Des mutants thermoresistants ont ete isoles a partir de la souche attenuee sabin 1 par des passages successifs a 37. 5#oc, 38. 5#oc et 39. 5#oc. La thermoresistance des quatre mutants etudies a ete confirmee par un test de multiplication a 35#oc et 40#oc. La neurovirulence a ete etudiee chez le singe et s'est averee positive pour tous les mutants (mutants isoles a 37. 5#oc: 2/4 singes paralyses; mutants isoles a 38. 5#oc et 39. 5#oc: 4/4 singes paralyses). Pour tenter d'etablir une correlation entre certaines mutations, la thermoresistance et la virulence, nous avons sequence de facon comparative le genome de la souche sabin 1 et des mutants thermoresistants. Nous avons choisi les regions ou ont ete observees des mutations entre la souche attenuee sabin 1 et la souche virulence mahoney (56 mutations ponctuelles). Nous avons donc sequence 80% du genome de chaque mutant et de la souche parentale sabin 1. Les mutants selectionnes a 39. 5#oc possedent deux mutations dans la region de vp1, une dans celle de vp3, une autre dans le gene de la polymerase virale et deux dans les regions 5 et 3 non codantes. Le mutant selectionne a 38. 5#oc possede la mutation observee dans le gene de la polymerase et les mutations des regions 5 et 3 non codantes. Le mutant selectionne a 37. 5#oc possede les 2 mutations des regions 5 et 3 non codantes. Le neurotropisme du poliovirus a d'autre part ete etudie in vitro dans des cellules de neuroblastome humain. Une infection persistante est etablie et les caracteres phenotypiques des virus persistants different de ceux des virus parentaux. Enfin, nous avons construit et etudie des mutants d'insertion du poliovirus qui portent un nouvel epitope immunogene sur leur capside

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Mallet, Laurent. "Analyse qualitative et quantitative des marqueurs moléculaires majeurs de la neurovirulence des poliovirus". Lyon 1, 1996. http://www.theses.fr/1996LYO1T195.

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Carsillo, Thomas John. "A role for the major inducible 70 KDA heat shock protein (HSP72) in experimental measles encephalitis". Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1141316578.

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Sabaratnam, Keshalini. "The interaction between the Marek's Disease Virus (MDV) neurovirulence factor pp14 and the host transcription factor, CREB3". Thesis, University of Oxford, 2017. http://ora.ox.ac.uk/objects/uuid:d2fc6bd4-bc3a-4a37-924b-86881096a9b5.

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Marek's Disease Virus (MDV) induces a wide range of neurological syndromes in susceptible hosts; however, the mechanisms behind the MDV-induced neuropathology are still poorly understood. The immediate-early 14kDa phosphoprotein, pp14, is associated with the neurovirulence phenotype of the virus. Yeast-two-hybrid screening identified the ER-bound transcription regulator, human CREB3 (cAMP Response Element-Binding protein), as an interacting partner of pp14, and fluorescence colocalisation between pp14 and chicken CREB3 (chCREB3) in MDV infected cells suggested an interaction between these proteins. The primary focus of this DPhil project was to further investigate this putative interaction using in vitro studies, with a view to determining if the interaction is linked to the neurovirulence of MDV. This investigation, which employed a combination of biochemical, cellular, and functional assays, found no conclusive evidence in support of the predicted interaction. In addition, this project aimed to gain structural and functional insights into the MDV neurovirulence factor pp14 and the host transcription factor, chCREB3. Biophysical characterisation of recombinant pp14B identifies pp14 as a molten globule. The results reveal the protein, while possessing substantial secondary structure, is largely disordered lacking a stable tertiary structure. Multiple lines of evidence from this study also indicate pp14 is a putative zinc-binding protein. Moreover, phosphorylation analysis of recombinant pp14B, extracted from DF1 cells, by mass spectrometry provides conclusive evidence for the presence of two phosphorylation sites in the shared C-terminal region of pp14 - serines 72 and 76 of pp14B. Structural flexibility, through a lack of a definite ordered tertiary structure, and functional features that can induce structural modifications indicate pp14 might interact with a number of binding partners and therefore could play multiple roles during MDV infection - a strong possibility due to the expression of the protein in all the different stages of virus infection. Furthermore, this thesis presents the crystal structure of the homodimeric chCREB3 bZIP. The chCREB3 bZIP possesses a structured DNA binding region even in the absence of DNA, a feature that could potentially enhance both the DNA-binding specificity and affinity of chCREB3. Significantly, chCREB3 has a covalent intermolecular disulphide bond in the hydrophobic core of the bZIP, which may play a role in promoting stability. Moreover, sequence alignment of bZIP sequences from chicken, human and mouse reveals only members of the CREB3 subfamily possess this cysteine residue, indicating it could act as a redoxsensor. These results indicate members of the CREB3 subfamily, by possessing a putative redox-sensitive cysteine with the capacity to form an intermolecular disulphide bond, may be activated in response to oxidative stress.

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Capítulos de livros sobre o assunto "Neurovirulence"

Agol, Vadim I. "Poliovirus Neurovirulence and its Attenuation". In Regulation of Gene Expression in Animal Viruses, 305–21. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2928-6_21.

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Jackson, A. C. "Animal Models of Rabies Virus Neurovirulence". In Current Topics in Microbiology and Immunology, 85–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78490-3_5.

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Levine, Myron, David J. Fink, Ramesh Ramakrishnan, Prashant Desai, William F. Goins e Joseph C. Glorioso. "Neurovirulence of Herpes Simplex Virus Type 1 Accessory Gene Mutants". In Pathogenicity of Human Herpesviruses due to Specific Pathogenicity Genes, 222–37. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-85004-2_13.

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Fujimura, R. K., P. Shapshak, D. M. Segal, K. A. Crandall, K. Goodkin, J. B. Page, R. Douyon et al. "Viral and Host Determinants of Neurovirulence of HIV-1 Infection". In Advances in Experimental Medicine and Biology, 241–53. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5347-2_27.

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Solomon, T., e P. M. Winter. "Neurovirulence and host factors in flavivirus encephalitis — evidence from clinical epidemiology". In Emergence and Control of Zoonotic Viral Encephalitides, 161–70. Vienna: Springer Vienna, 2004. http://dx.doi.org/10.1007/978-3-7091-0572-6_14.

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Power, C., J. C. McArthur, R. T. Johnson, D. E. Griffin, J. D. Glass, R. Dewey e B. Chesebro. "Distinct HIV-1 env Sequences Are Associated with Neurotropism and Neurovirulence". In Current Topics in Microbiology and Immunology, 89–104. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79657-9_7.

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Matsuyama, Shutoku, Rihito Watanabe e Fumihiro Taguchi. "Neurovirulence for Mice of Soluble Receptor-Resistant Mutants of Murine Coronavirus JHMV". In Advances in Experimental Medicine and Biology, 145–48. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1325-4_23.

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Wege, H., J. Winter, P. Massa, R. Dörries e V. ter Meulen. "Coronavirus JHM Induced Demyelinating Disease: Specific Domains on the E2-Protein are Associated with Neurovirulence". In Coronaviruses, 307–20. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-1280-2_40.

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Taguchi, Fumihiro, Hideka Suzuki, Hiromi Takahashi e Hideyuki Kubo. "Neurovirulence for Rats of the JHMV Variants Escaped from Neutralization with the S1-Specific Monoclonal Antibodies". In Advances in Experimental Medicine and Biology, 185–87. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1899-0_31.

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Ben-Nathan, D., S. Lustig e G. Feuerstein. "The Effect of Cold or Isolation Stress on Neuroinvasiveness and Neurovirulence of an Avirulent Variant of West Nile Virus (WN-25)". In Psychiatry and Biological Factors, 295–306. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5811-4_27.

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