Tesi sul tema "Herpèsvirus équin de type 1"
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Carnet, Flora. "Amélioration des protocoles vaccinaux contre la grippe équine et la rhinopneumonie : apport de l’iPPVO en tant qu’adjuvant dans le modèle équin, nouvelle approche de la mesure des anticorps neutralisants". Electronic Thesis or Diss., Normandie, 2023. http://www.theses.fr/2023NORMC413.
Equine influenza virus (EIV) and equine herpesvirus-1 (EHV-1) are frequently described in many countries and are two endemic pathogens in the French equine population. These infectious diseases have important consequences both in terms of animal health and welfare and in terms of economic impact. The fight against these viruses is essentially based on the implementation of preventive measures such as vaccination. Despite this epizootics of EIV and EHV-1 are regularly declared in France and throughout the world. Neutralising antibodies, synthesised in response to infection or after immunisation, represent the main line of defence against these viruses. Improved vaccines and a wider range of tools to measure neutralising antibodies can be a valuable strategy in the fight against these viruses. In order to improve the efficacy of the vaccine response, both in magnitude and duration, the use of adjuvants is one way to improve immunogenicity. This thesis consisted, in the first instance, in establishing the proof of concept of the use of iPPVO as an innovative adjuvant in vivo in horses in the context of vaccination against EIV. For this purpose, antibodies were measured by SRH, a method for which the correlates of protection are well defined. The addition of iPPVO at vaccination significantly increased the antibody level to EIV and protection in horses up to 6 months after immunisation. In a second step, a new method for measuring EIV antibodies in serum based on impedancemetry was developed to improve on current methods and facilitate high throughput analysis. This neutralisation test correlated well with SRH test. Another study was performed, which demonstrated the adjuvant potential of iPPVO in horses during vaccination against EHV-1,4. The antibody response measured by serum neutralisation increased up to 5 months after immunisation. Finally, preliminary results on the mechanism of action of iPPVO on peripheral blood mononuclear cells demonstrated the importance of the interferon
Geoffroy, Marie-Claude. "Réactivation de l'expression du gène rep de l'Adeno-Associated Virus de type 2 par la protéine ICP0 de l'Herpès Simplex de type 1". Nantes, 2005. http://www.theses.fr/2005NANT16VS.
Adeno-associated virus type 2 (AAV-2) is a human parvovirus that requires the presence of a helper virus, such as the herpes simplex virus type 1 (HSV-1) to accomplish a complete productive cycle. In the absence of helper virus, AAV-2 can establish a latent infection that is characterized by the absence of expression of viral genes. So far, four HSV-1 early genes, UL5/8/52 (helicase primase complex), and UL29 (ssDBP), were defined as sufficient for AAV replication when cells were transfected with a plasmid encoding for the wild type AAV-2 genome. However, none of these viral products was shown to behave as a transcriptional factor able to activate AAV gene expression. Our study provides the first evidence that the immediate-early HSV-1 protein ICP0, can promote rep gene expression in cells latently infected with wild type AAV-2. This ICP0-mediated effect occurs at the transcriptional level and involves the ubiquitin-proteasome pathway. Furthermore, using deletion mutants we demonstrate that the localization of ICP0 to ND10 and their disruption is not required for the activation of the rep promoter. Finally, ubiquitin-specific protease USP7 plays an indirect role in the reactivation of rep gene expression. Altogether, this study indicates that ICP0 is a key helper factor for AAV gene activation and thus contributes to the definition of the HSV-1 helper activities
Pronost, Stéphane. "Apports des outils de génétique moléculaire à la connaissance de deux infections virales du cheval : herpèsvirus équin 1 et artérite virale équine". Caen, 2010. http://www.theses.fr/2010CAEN3120.
Many viruses are responsible of equine pathologies and may involve both outbreaks and trade limitations. Among them, equid herpesvirus -1 (EHV-1) and equine arteritis virus (EAV) are monitored closely. Methods of detection and molecular characterisation were developed. We investigated the relationships between the different clinical expressions of EHV-1 infection and genotype of the strains being present in France. We could confirm EHV-1 being both a major abortive agent and also responsible of either sporadic or epidemic neurological diseases. Determining by SNP-PCR the presence/absence of mutation A/G2254 in ORF 30, coding for DNA polymerase, allowed to precise that non-neuropathogenic strains could be detected during paralytic forms, and conversely, neuropathogenic strains could be detected during abortive forms of the disease. This suggests that other factors related to horse and environment also are interfering with the clinical expression of the syndrome. Characterisation of the French strains of EAV, by phylogenetic analyses of ORF 2a-7, allowed demonstrating the emergence in 2003 of a North American strain. The outbreak of equine viral arteritis being described in this paper, revealed an European strain from subgroup 2 (highly virulent) to be responsible of one abortion and death of seven horses. Perspectives are based on the complete sequencing of EHV-1 genome as well as phylogenetic study of other EAV strains in order to determine the origin of the outbreak
Zaupa, Cécile. "Développement et utilisation de nouveaux outils biologiques basés sur l'emploi du système de recombinaison Cre/loxP afin de produire des vecteurs amplicons non cytotoxiques dérivés du virus de l'Herpès Simplex de type I". Lyon 1, 2003. http://www.theses.fr/2003LYO10035.
Morency, Eric. "The protein of herpes simplex virus Type 1 : from centromeres to the interphase centromere damage response". Lyon 1, 2007. http://www.theses.fr/2007LYO10317.
Beitia, Ortiz de Zárate Igor. "Etude du transport intracellulaire de la Glycoproteine B de HSV-1 et de son impact sur l'infection virale". Paris 7, 2006. http://www.theses.fr/2006PA077071.
Herpes simplex virus type 1 (HSV-1) is a human pathogen which infects neurons and can reach the central nervous System (CNS), causing encephalitis. Glycoprotein B (gB), a main component of HSV-1 necessary for entry into host cells, has been involved in neuroinvasion. Its cytoplasmic domain contains highly conserved motifs, similar to motifs involved in intracellular sorting of transmembrane proteins. To determine their role in the intracellular transport and maturation of gB, we deleted or mutated these motifs, and characterized the subsequent modifications in transfected and infected cells. We identified a region that includes the di-acidic motif ERTE, which is essential for the maturation and cell surface expression of gB, and for complementation of a gB-null virus. Two other motifs, YTQV and LL, participate in the retrograde transport of gB from the cell surface to the TGN. Whereas YTQV is essential for internalization of gB from the cell surface, LL most likely participates in a further step of this transport, since mutation of the LL motif does not prevent internalization of gB, but delays its accumulation in the TGN, while enhancing its recycling to the cell surface. Modification of these motifs leads to a decrease in virus infectivity and to changes in the phenotype of infection in cell culture (disruption of the LL motif enhances syncytium formation and the opposite is observed when the YTQV motif is modified). Altogether, these results favor a model in which HSV-1 gets its glycoproteins and final envelope at the TGN, and suggest that retrograde transport of gB, albeit non essential, might play an important role in cell-to-cell spread and infectivity of the virus
Cuchet, Delphine. "Développement de vecteurs dérivés du virus de l'herpès simplex de type (HSV-1) pour le traitement des tumeurs cérébrales". Lyon 1, 2004. http://www.theses.fr/2004LYO10114.
HSV-1 derived vectors are promising tools for viral oncolysis or gene therapy by suicide gene of brain tumors. Attenuated recombinant vector are used for viral oncolysis. We have constructed and characterized a recombinant vector which carries a transgenic, biscistronic and auto-inductible expression unit. Defectif amplicon type vectors are tools with good potential for transfer of large size DNA in variety of cell types. We have constructed and developed an amplicon vector which carries the gene encoding the herpetic ICP0 protein. Human glioblastoma cells infected with this vector stop proliferating, resulting in cell death. No toxic effects were observed in non proliferaing infected cells. We have studied the expression of a second transgene carried by amplicon vectors and showed that though its expression is cell type dependent, simultaneous ICP0 expression could significantly increased it
Mahiet, Charlotte. "Caractérisation du génome de l'herpès simplex virus de type 1". Paris 7, 2012. http://www.theses.fr/2012PA077069.
HSV-1 is a prevalent human pathogen that commonly leads to recurrent facialoral lesions. Although there are efficient drugs to block its replication, HSV-1 is never clear of the host Within this context, the company Cellectis aims to develop a new class of therapeutic agent (the meganucleases) that specifically cleaves into the HSV-1 genome of infected cells, thus allowing its eradication. The first question addressed during this thesis was how to assess the efficacy and safety of such a therapy. We proposed molecular combing for the direct visualization and analysis of single DNA molecules through hybridization of specific probes on uniformly and irreversibly stretched HSV-1 DNA. Following technical improvements, we successfully detected the genomes in viral particles and infected cell DNA extracts, as well as in DNA extracts from mouse, rabbit and human cornea. We were confronted to the complexity of the organization of HSV-1 genomes. Indeed, its 152 kb genome is organized in two covalently linked-segments. Each segment is composed of a unique sequence flanked by inverted repeated sequences. During replication, four HSV-1 genome isomers are produced by homologous recombination between the inverted repeats. We tested the hypothesis that the process of isomerization systematically results in a random distribution no matter which cell or strain is considered. Using HSV-1 probes, we were able to distinguish between the four isomers through molecular combing analysis. Interestingly, both in vitro and in vivo, we found imbalanced distribution functions of the strain, cell or tissue considered. In the DNA extract of infected cells, concatemeric molecules as long as 10 equivalent genomes were detected. Strikingly, among these, the isomers distribution was always equivalent. This suggests that any such imbalance may occur during encapsidation. A considerable proportion of non-canonical assortments were detected in vitro and in vivo
Savard, Nathalie. "Production de vecteurs rétroviraux à l'aide de vecteurs herpétiques de type amplicon". Lyon 1, 1996. http://www.theses.fr/1996LYO10299.
Bataille, Dominique. "Analyses de la structure des intermédiaires de la réplication de l'ADN du virus Herpes simplex de type 1". Lyon 1, 1997. http://www.theses.fr/1997LYO10146.
Epstein, Alberto-Luis. "Le virus de l'Herpes simplex de type 1 : étude des facteurs viraux et cellulaires en relation avec l'infection abortive in vitro". Lyon 1, 1985. http://www.theses.fr/1985LYO10029.
Simonin, Denis. "Régulation post-transcriptionnelle de l'expression génique dans les cellules infectées par le virus de l'herpès simplex de type 1". Lyon 1, 1995. http://www.theses.fr/1995LYO1T101.
Lamigeon, Cyrile. "Amélioration de la capacité antioxydante de différentes cellules du système nerveux central après transfert du gène codant pour la glutamate décarboxylase". Lyon 1, 2002. http://www.theses.fr/2002LYO1T236.
Fournel-Garcia, Sandrine. "Mise au point et analyse de vecteurs herpétiques de type amplicon destinés au transfert de gène dans les cellules eucaryotes". Lyon 1, 1996. http://www.theses.fr/1996LYO10085.
Masse, Thierry. "Régulation traductionnelle de l'expression génétique dans des cellules infectées par le virus Herpes simplex de type 1 : définition d'un modèle expérimental". Lyon 1, 1990. http://www.theses.fr/1990LYO10150.
Cloutier, Nathalie. "Rôle des protéines de latence du virus humain herpès-8 sur la synthèse d'interféron de type 1". Thesis, Université Laval, 2010. http://www.theses.ulaval.ca/2010/27219/27219.pdf.
Laurent, Anne-Marie. "Régulation traductionnelle de l'expression génique cellulaire et virale après infection par le virus herpes simplex de type 1". Lyon 1, 1998. http://www.theses.fr/1998LYO1T043.
Crépin, Sophie. "Comparaison de modèles murins de la maladie herpétique selon la souche virale et le site d'inoculation". Paris 11, 2009. http://www.theses.fr/2009PA114805.
Herpes simplex virus type 1 (HSV 1) is able to establish latent infection in neuronal tissues after a oral primary infection. Spontaneously or upon stimuli, HSV1 can reactive and induce ocular disease. The mechanisms involved in balance between latent infection and reactivation are not completely understood. In oro-ocular murin model of HSV1 (strain SC16) infection, the amounts of Latent-Associated Transcripts (LATs) and non-sliced ICPO transcripts, which encodes a protein involved in the reactivation process, have a similar pattern of evolution from the acute to the latent stage of infection, with an accumulation in trigeminal ganglia and a decrease in other latency sites. Such striking difference between types of neurones was partially found in the corneal scarification model of HSV1 infection. But, classical patterns of HSV1 latency, i. E. Complete extinction of early and late viral genes expression was not obtained in this model, especially with the KOS strain of HSV1. These results suggest that the biological patterns of HSV1 latency depend on the type of neurons, the viral strain and the murin model
Cassar, Olivier. "Epidémiologie et variabilité génétique des virus HTLV-1 et HHV-8 dans l'archipel du Vanuatu : contribution à l'étude des migrations humaines en Mélanésie". Paris 7, 2008. http://www.theses.fr/2008PA077024.
In this study we demonstrate, for the first time, by molecular analysis the presence 0f htlv-1 genome in 41 htlv-1 seropositive vanuatu inhabitants. The sequence analysis clearly showed that these strains belong to the divergent molecular subtype c. These htlv-1 variants should be representative of the strains present in whole vanuatu population. Molecular clock analysis showed that these strains were probably introduced during ancient migration of the original settlers, 10 000 years ago. We also show human herpesvirus 8 with diverse molecular subtype d variants to be highly endemic among the vanuatu populations. Most kl genes were nearly identical to polynesian strains, although a few clustered with australian or taiwanese strains. Taken together, these results suggest diverse origins of the vanuatu populations and raise questions about the ancient human population movments in melanesia. Further molecular studies about mitochondrial dna of the infected populations are now ongoing and well help us to reconstruct the patterns of human dispersal into oceania
Chapgier, Ariane. "Human STAT1 deficiencies". Paris 7, 2007. http://www.theses.fr/2007PA077079.
The Signal Transducer and Activator of Transcription 1 (STAT1) is activated in response to Interferons (IFNs) stimulations. In response to IFN-y, STAT1 homodimerizes to form an activator of transcription: theche gamma activating factor (GAF). In response to IFN-α, STAT1 heterotrimerizes with STAT2 and ISGF3γ to form an activator of transcription: the interferon sequence gene factor 3 (ISGF3). This thesis work first clearly demonstrates the role of the IFN-γ-induced-GAF complexes in anti-mycobacterial immunity and the role of IFN-α-induced-ISGF3 complexes in the anti-viral immunity. Second, this work characterizes all STAT1 human mutations and demonstrates there was no haploinsufficiency of STAT1 for GAF and ISGF3 activations. Patients homozygous for STAT1 mutations present mycobacterial and viral diseases. These mutations are ail associated with defect of STAT1 expression leading to defects in both GAF and ISGF3 activations. Patients heterozygous for STAT1 mutations present only mycobacterial diseases. Their respective mutations are not associated with defects of STAT1 expression, but of its inducible phosphorylation or DNA binding activity upon IFNs stimulations. These mutated alleles are associated with defects in only GAF activation in patient's heterozygous cells. They are dominant for the IFN-y-induced-GAF mediated anti-mycobacterial immunity and recessive for the IFN-α-induced-ISGF3 mediated anti-viral immunity at the cellular and clinical level by different mechanisms. Therefore, this work thirdly highlights the importance in the candidate gene approach of whether the organism studied is heterozygous or homozygous for the mutation. It also highlights the fact that a phenotype depends not only of the affected gene but mainly of the mutation in this gene
Lussignol, Marion. "Caractérisation d’une nouvelle fonction de la protéine Us11 dans l’échappement à l’autophagie par le virus Herpès Simplex de type 1". Thesis, Paris 11, 2013. http://www.theses.fr/2013PA114807.
Autophagy is an evolutionary conserved vacuolar mechanism allowing to degrade cytoplasmic components and to maintaining cellular homeostasis, but it can also be triggered by a variety of stress-related conditions, including viral infection. The herpes simplex virus 1 (HSV-1) is able to counteract this antiviral mechanism. Notably, HSV-1 encodes a protein, IPC34.5, which inhibits autophagy through its interaction with the autophagy machinery protein Beclin 1. In the present work, we uncovered a second anti-autophagic protein from HSV-1, the late protein Us11, which likely plays a complementary role to ICP34.5 regarding the inhibition of autophagy by the virus. We demonstrated that ectopic expression of Us11 inhibited autophagy triggered by different stimuli, as observed for ICP34.5. Moreover, during viral infection, early expression of Us11 was sufficient to block autophagy in cells infected with a ICP34.5 virus, similarly to the wild-type virus. We then explored the mechanism of action of Us11. Us11 has been described as capable of interacting with the dsRNA-dependent kinase PKR, therefore preventing it to phosphorylate its substrate eIF2, a translation initiation factor. We demonstrated that Us11 was no longer able to inhibit autophagy when expressed in PKR-deficient cells. We confirmed that Us11 binding to PKR was necessary for its function by constructing various truncated forms of Us11 that showed that the PKR-binding domain was crucial. We also unveiled the importance of a domain located within the N-terminal part of Us11. This domain has no cellular molecular partner known, but it can allow Us11 to interact with another protein of the autophagy machinery. However, we further showed that Us11 did not interact with Beclin 1 nor affected the kinase activity of mTOR, another important pathway regulating autophagy. In our work, we also gained insights into regulatory mechanisms of starvation-induced autophagy.The inhibition of autophagy through the specific blockade of PKR by Us11 had never been previously described. This work thus paves the way for studying the involvement of PKR/eIF2 pathway in the regulation of autophagy and for exploring the role of autophagy in HSV-1 neurovirulence
Aouacheria, Abdel. "Transformation cellulaire par l'oncogène v-Src et caractérisation des homologues de la protéine de survie Nr-13". Lyon 1, 2002. http://www.theses.fr/2002LYO1T110.
Pourchet, Aldo Decio. "Développement de virus HSV-1 (virus de l’herpes simplex de type 1) oncolytiques ciblés pour traiter les carcinomes hépatocellulaires". Thesis, Lyon 1, 2010. http://www.theses.fr/2010LYO10155/document.
Our long-term purpose is to develop transcriptionally targeted oncolytic vectors, derived from herpes simplex virus type 1 (HSV-1), designed to eradicate hepatocellular carcinomas (HCC). We have identified several HCC-specific promoters, as well as other cancer-specific promoters, that maintain their specificity when expressed from the virus genome. More precisely, we have demonstrated that these promoters are able to drive reporter gene (luciferase) expression from the virus genome in HCC-derived cells, both in cultured cells and in nude mice, but not in fresh human hepatocytes or in the WRL38 hepatocyte-like cells. HSV-1 infection induces, but then inhibits, a cellular antiviral apoptotic response, and the early virus protein US3 is a key actor in inhibiting apoptosis. We have hypothesized that inhibition of US3 expression in hepatocytes should led to early apoptotic death of these cells, therefore precluding virus multiplication and spread. In contrast, expression of US3 in cancer cells is expected to block apoptosis, leading to the achievement of the virus life cycle, cell lysis, and virus spread within the tumours. We report in this communication the construction and properties of two different potentially oncolytic HSV-1 vectors. One of them expresses US3 protein under the control of the HCC-specific promoter ANGPTL3, while the second promoter contains 9 repeats of the hypoxia responsive elements of vascular-endothelial growth factor (VEGF) (9xHRE promoter). Growth curves of these viruses were performed on different HCC cell lines to show their oncolytic properties
Maillet, Séverine. "Étude de l'expression des gènes IE110 et LAT (Latency Associated Transcript) du virus herpes simplex de type 1 (HSV1) lors de la phase de latence dans le modèle murin de primo-infection herpétique orale". Paris 11, 2005. http://www.theses.fr/2005PA114829.
Masy, Eric. "Rôle de la protéine LMP-1 du virus d'Epstein-Barr (EBV) dans la prolifération de cellules présentant une latence virale de type II : caractérisation d'une lignée monocytaire transformée par le virus". Lille 2, 2002. http://www.theses.fr/2002LIL2P006.
Berry, Noémie. "Le stress mitochondrial induit par le Virus de l’Herpès Simplex de type 1 entraîne la surexpression de la cytidine désaminase APOBEC3A". Electronic Thesis or Diss., Sorbonne université, 2019. http://www.theses.fr/2019SORUS185.
The presence of DNA in the cytosol represents a danger signal. Mitochondrial DNA (mtDNA) has been recognized as a DAMP (damage-associated molecular-pattern molecule), able to induce the production of pro-inflammatory cytokines (interferons). The human cytidine deaminase APOBEC3A (A3A), upregulated by IFN, catalyzes the deamination of cytidine to uridine in single stranded DNA substrates leading to the catabolism of the mutated DNA sequence and the suppression of the signal. First, we demonstrated the role of the RNA polymerase III / RIG-I signaling in the upregulation of A3A expression in response to IFN production. We also confirmed the mtDNA catabolism induced by A3A. However, its overexpression leads to GC vers AT mutations and double-strand DNA breaks in the nuclear genome. The second part of my thesis highlighted the release of mtDNA within the cytosol upon Herpes Simplex Virus Type 1 (HSV-1) infection in a human cellular model, probably triggered by a fragmentation of the mitochondrial network. We demonstrated that this mtDNA release is associated with a strong production of IFN and the overexpression of A3A. While we confirmed the role of the RNA polymerase III / RIG-I signaling, the cGAS-STING pathway should be also involved. Finally, in this thesis, we have shown in a human model that the mitochondrial stress induced by HSV-1 contributes to the overexpression of A3A
Rousseau, Antoine. "Cinétique des effecteurs immunologiques impliqués dans la protection contre le virus Herpès simplex type 1 (HSV1) après primo-infection par une autre souche non neurovirulente : vers un modèle vaccinal". Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS339.
In humans, Herpes simplex virus type 1 (HSV-1), primary infection occurs in the oral mucocutaneous tissues. Virions replicated here penetrate sensitive neuronal axons, migrate to both trigeminal ganglion (TG) where it established a lifelong latency. Reactivations of HSV-1 in the TG neurons induce clinical recurrences in the connected peripheral tissues. This process is involved in herpes simplex keratitis (HSK), a condition that, strikingly, occurs almost exclusively in the same eye for a given patient. Based on an experimental oro-ocular (OO) model of HSV-1 infection, that recapitulates most of these human clinical features, we previously demonstrated that a virus inoculation on one side of the mouth, leads to viral replication in the lip, followed by HSK. Virus concomitantly disseminates to both TG, but reactivation only occurs in the TG ipsilateral to the inoculation site. We also observed that after a primary inoculation with a non-neurovirulent strain of HSV-1 in one lip, mice are protected against both acute phase disease and reactivation after a superinfection with a fully virulent wild-type strain of HSV-1 in the contralateral lip.In order to understand the underlying mechanisms involved in this state of protection, we combined high resolution flow cytometry and bead-based immunoassays, to quantify hematopoietic subsets and inflammatory chemokines in the site of inoculation and in the TG. We demonstrated that after a single inoculation with the wild-type strain, a delayed immune infiltrate, boasting more proinflammatory subsets, occurred in the lip and persisted in the TG. In contrast, the immune infiltrate occurred earlier in the superinfected lip and ipsilateral TG, with less inflammatory chemokines but more adaptive immune subsets. Moreover, cellular infiltrate resolved faster, correlating with nullification of inflammatory chemokines locally. These data show that immune response kinetics influence the development of natural immunity to HSV-1, and can be harnessed to protect against disease and reactivations
Hippocrate, Aurélie. "Modulation de l'autophagie lors de la réactivation de l'EBV par le TGF β1". Paris 7, 2011. http://www.theses.fr/2011PA077182.
The Epstein-Barr virus (EBV) is a persistent gamma herpesvirus, which is associated with malignancies. The requirement of lytic gene expression for outgrowth of lymphoproliferations in a SCID mouse model, suggests the importance of reactivation for EBV pathogenesis. Transforming Growth Factor beta 1 (TGF-pl) induces EBV reactivation. During TGF-pl-mediated EBV reactivation, an autophagy inhibitor, PI3K/Akt, was activated, and an autophagy inducer, the interferon-inducible protein kinase activated by double-stranded RNA (PKR), was inactivated. This prompted us to investigate the effect of TGF-pl-mediated viral reactivation on the autophagy process. Autophagy markers were decreased after treatment by TGF-pl of EBV-infected Burkitt's lymphoma (BL) cell lines and not in EBV negative BL cells showing an EBV-dependent inhibition of autophagy during TGF-pl mediated EBV reactivation. The autophagic pathway is a cellular defence process involving the bulk degradation of cellular contents by autophagosomes/lysosomes during starvation or viral infection and autophagy is postulated to play a role in antiviral innate immunity. Inhibition of autophagy might prevent cellular antiviral defence. Elucidating the molecular mechanisms which lead to EBV reactivation (deregulation of autophagy, apoptosis and signals involved) will be important to understand its association with the development and / or progression of malignant lymphomas
Nagy, Héléna Juliana. "Traitement des tumeurs hépatiques et ovariennes expérimentales par transfert de gène codant pour la thymidine kinase du virus herpès simplex de type 1". Paris 5, 1999. http://www.theses.fr/1999PA05CD03.
Thieulent, Côme. "Criblage in vitro de molécules antivirales contre l'herpèsvirus équin-1 par impédancemétrie et évaluation clinique de l'effet du valganciclovir Screening and evaluation of antiviral compounds against Equid alpha-herpesviruses using an impedance-based cellular assay Identification of antiviral compounds against equid herpesvirus-1 using real-time cell assay screening: Efficacy of decitabine and valganciclovir alone or in combination Screening of potential antiviral molecules against equid herpesvirus-1 using cellular impedance measurement: dataset of 2,891 compounds New EHV-1 variant identified | Veterinary Recordvir réduit les signes cliniques, l'excrétion virale et la virémie chez des poneys infectés expérimentalement par la nouvelle souche C2254 d'herpèsvirus équin 1 Oral administration of valganciclovir reduces clinical signs, virus sheedind and cell-associated viremia in ponies experimentally infected with the new variant C2254 of equid herpesvirus-1". Thesis, Normandie, 2020. http://www.theses.fr/2020NORMC421.
Nine herpesviruses are known to infect the equine population. Among them, the equid herpesvirus 1 (EHV-1) induces the most severe forms of diseases. Indeed, this virus causes respiratory symptoms, abortions, neonatal foal deaths and nervous diseases, often leading to their euthanasia. Prophylaxis, relying on good sanitary practices and vaccination remains the best way to avoid epizooties of herpesviruses. Vaccines reducing efficiently respiratory disorders and EHV-1 dissemination are currently available. However, they do not prevent abortions and have no proven effect against nervous symptoms. In addition, the vaccine coverage is insufficient in France. Antiviral therapy is therefore an interesting complementary approach in the fight against EHV-1. However, there is a lack of studies evaluating the antiviral effect of compounds against EHV-1, limiting the prospects of use. To resolve this issue, we have developed a medium/high throughput screening protocol using the RTCA xCELLigence® technology based on cell impedance measurements. Following the screening of 2891 compounds, 21 candidates were identified for their efficacy against EHV-1. Among them, aphidicolin, decitabine, ganciclovir, idoxuridine, pritelivir and valganciclovir showed the best efficacy. The activity of these compounds was confirmed on different cell lines in the presence of different EHV-1 strains. This study led to the identification and the understanding of the mode of action of decitabine. This deoxycitidine analogue, also showed a synergistic effect when combined with valganciclovir. In the second part of this work, we evaluated the effect of valganciclovir treatment during an experimental infection by nebulisation with a new EHV-1 strain (C2254) recently isolated during the epizootic of 2018. This study demonstrated that a dose of 6.5 mg/kg body weight of valganciclovir, administrated orally twice a day, allowed to maintain a good protection prior the establishment of the humoral immune response. Indeed, this treatment allows to reduce significantly clinical signs, viral excretion and cell-associated viremia induced by EHV-1 on ponies. This work carried out in vivo demonstrated the efficiency of valganciclovir treatment against EHV-1, while the in vitro screening opens up new perspectives of treatment, in particular with compounds association
Zhang, Shen-Ying. "Herpes simplex encephalitis in children : deficiences in Toll-Like receptor 3 signalling pathway". Paris 5, 2007. http://www.theses.fr/2007PA05T016.
Gross, Sylvain. "Etude de la déstabilisation des structures protéique et chromatinienne des centromères par la protéine ICP0 du virus Herpes Simplex de Type 1". Phd thesis, Université Claude Bernard - Lyon I, 2011. http://tel.archives-ouvertes.fr/tel-00838586.
Albaret, Marie Alexandra. "Rôle potentiel du virus herpes simplex de type I dans la maladie d'Alzheimer". Thesis, Lyon 1, 2009. http://www.theses.fr/2009LYO10117.
The origin of the sporadic form of the Alzheimer's disease (AD) remains still widely unknown. However, an adequacy between environmental and genetic factors is highly probable. Numerous arguments suggest that the virus herpes simplex of type 1 (HSV1) by infecting and replicating in the central nervous system, could be a co-factor involved in the AD process. To evaluate this hypothesis, we set up a model made of rat neurons infected by HSV1 in order to analyse the virally-induced modifications of their gene expression. Using this model we have shown: i) an over-production of the amyloid peptide Aß42 and of phosphorylated form of Tau accompanied by their concentration within an intracellular aggresome; ii) variations of the transcription levels of numerous genes equivalent to that observed in AD patients. Furthermore, the study of the molecular mechanisms underlying the virally-induced apoptosis allowed to point out a correlation between caspase activation and Aß42 production as well as a correlation between abortosis and aggresome formation. All together these results demonstrate that this cellular model represents, at least in part, some aspects of the early stages of AD and bring evidences that HSV1 could be a co-factor in the AD process
Thevenin, Thomas. "Pouvoir virucide de désinfectants à l'encontre de coxsackievirus B4 et d'autres virus en suspension ou en surface". Thesis, Lille 2, 2011. http://www.theses.fr/2011LIL2S052.
The resistance of viruses to drying relies on several factors : the type of surface, temperature, humidity and the compositon of the viral envelope or capsid. A virus adsorbed on a surface can remain infectious for several days or months if the conditions are met. [...] In this thesis, methods were developed to compare the virucidal activity of disinfectants towards viruses in suspension and on surfaces (stainless steel or non-woven fuctionalized textiles). Two approaches were implemented : the first to test the virudical activity of functionalized surfaces
Firquet, Swan. "Inactivation virale par méthodes physiques". Thesis, Lille 2, 2014. http://www.theses.fr/2014LIL2S048/document.
The pattern of viability of non-enveloped viruses, minute virus of mice (MVM), coxsackievirus B4 (CVB4), and simian virus 40 (SV40) and enveloped-viruses, influenza A virus (H1N1), and herpes simplex virus type 1 (HSV-1) onto surfaces and their resistance to heating and to ultraviolet C (UVc) exposure have been investigated. To determine the viability of MVM, CVB4, H1N1 and HSV1 on surface, fifty microliters of viral suspension were applied onto petri dish lids and dried under air flow of biosafety cabinet. The recovered viral preparations were titered on appropriate cell cultures. Enveloped viruses persisted for less than 5 days while CVB4 and MVM persisted for weeks. However, repetitive cycles of drying and resuspension had more virucidal effect on CVB4 than on H1N1 and HSV-1. No effect of these repetitive cycles on infectious titer of MVM was recorded. When exposed to drying, initial concentrations of bovine serum albumin, foetal calf and sodium chloride (NaCl) had an impact on the viability of CVB4. In a protein rich medium, CVB4 was more likely inactivated by drying whereas in presence of NaCl, the impact of drying was reduced. Thus, it appears that the resistance of viruses toward drying is not due to a heterogeneity of viral populations, but it can be influenced by media composition and components concentrations.Heat inactivation of viruses was reported, however, the thermal resistance of viruses in droplets has not been studied. We evaluated the pattern of heat resistance of MVM, CVB4, H1N1 and HSV1 contained in droplets. Four microliters droplets containing viruses were applied onto warmed surface obtained by using a self-made heating device. Viral suspensions were exposed to temperatures ranging from 70 to 130°C for 0 to 90 min depending on the virus, and then the recovered viral preparations were titered. Clearly, MVM was more resistant than H1N1 that was more resistant than HSV-1 and CVB4. For the first time, the inactivation of viral particles contained in drops exposed to temperatures higher than 100°C has been investigated. It appears that heating can have an unexpected faster virucidal effect than previously described. The resistance to ultraviolet C (UVc) (254nm) of MVM, CVB4, H1N1, HSV-1 and SV40 contained in droplets has been evaluated. Double-stranded DNA viruses (HSV-1 and SV40) were still infectious after exposure to 60 mJ/cm² UVc, while RNA viruses H1N1, CVB4 and single-stranded DNA virus MVM were fully inactivated when they were exposed to a dose equal to or lower than 35 mJ/cm² UVc. Moreover the effect of UVc (254 nm) combined with heating onto the viability of MVM was determined. The infectious level of MVM suspension droplets applied onto petri dish lids was fully inactivated when exposed to 27 mJ/cm² UVc. Heating (100°C for 20s) provoked a moderate reduction of infectious level (-1.8 log10TCID50) of MVM, whereas heating followed by UVc exposure (17 mJ/cm²) resulted in a full inactivation.In conclusion, our studies show that viruses can persist for days or even weeks on dry hydrophobic surfaces. The pattern of resistance of viruses toward drying is not due to a heterogeneity of viral population as shown by results obtained with CVB4. In so far as media composition play a role in the viability of viruses exposed to drying, the persistence of viruses in natural media (clinical or environmental), instead of defined media, should be investigated. The impact of short time exposure to heat onto the infectivity of viruses contained in a small volume of suspension has been determined. The thermal resistance of H1N1 up to 100°C, higher than the one of HSV1 another enveloped virus, and CVB4 a non-enveloped virus has been observed. An efficient viral inactivation can be obtained by combining UVc exposure and heating as shown by results obtained with MVM