Literatura científica selecionada sobre o tema "Virus – Reproduction (biologie)"
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Artigos de revistas sobre o assunto "Virus – Reproduction (biologie)"
Kennedy, Anissa, Jacob Herman e Olav Rueppell. "Reproductive activation in honeybee ( Apis mellifera ) workers protects against abiotic and biotic stress". Philosophical Transactions of the Royal Society B: Biological Sciences 376, n.º 1823 (8 de março de 2021): 20190737. http://dx.doi.org/10.1098/rstb.2019.0737.
Texto completo da fonteUddin, Mohammed Nizam, Sofi Mahmud Parvez, H. M. Shahadat Ali, Muhammad Samsuddin e A. N. M. Rezaul Karim. "Mathematical modeling on the transmission of COVID-19 and its reproduction numbers in SAARC countries". Journal of Applied and Natural Science 14, n.º 2 (18 de junho de 2022): 469–76. http://dx.doi.org/10.31018/jans.v14i2.3398.
Texto completo da fonteG, Gulothungan, Vickram A S e Kuldeep Dhama. "Angiotensin Converting Enzyme 2 (ACE2) - A macromolecule and its impact on human reproduction during COVID-19 pandemic". Journal of Experimental Biology and Agricultural Sciences 10, n.º 5 (31 de outubro de 2022): 960–77. http://dx.doi.org/10.18006/2022.10(5).960.977.
Texto completo da fonteMANDELBROT, LAURENT, e ROGER HENRION. "Human Immunodeficiency Virus and Reproduction". Annals of the New York Academy of Sciences 626, n.º 1 Frontiers in (junho de 1991): 484–501. http://dx.doi.org/10.1111/j.1749-6632.1991.tb37941.x.
Texto completo da fonteValansi, Clari, David Moi, Evgenia Leikina, Elena Matveev, Martín Graña, Leonid V. Chernomordik, Héctor Romero, Pablo S. Aguilar e Benjamin Podbilewicz. "Arabidopsis HAP2/GCS1 is a gamete fusion protein homologous to somatic and viral fusogens". Journal of Cell Biology 216, n.º 3 (30 de janeiro de 2017): 571–81. http://dx.doi.org/10.1083/jcb.201610093.
Texto completo da fonteRybalko, S., N. Nesterova, S. Diadiun, G. Danylenko, V. Danylenko, S. Guzhova, Y. Maksimov et al. "Therapeutical effect of modified adamantane copolymer compounds: study of molecular mechanisms." Acta Biochimica Polonica 48, n.º 1 (31 de março de 2001): 241–49. http://dx.doi.org/10.18388/abp.2001_5132.
Texto completo da fonteHarb, Julien, Nour Debs, Mohamad Rima, Yingliang Wu, Zhijian Cao, Hervé Kovacic, Ziad Fajloun e Jean-Marc Sabatier. "SARS-CoV-2, COVID-19, and Reproduction: Effects on Fertility, Pregnancy, and Neonatal Life". Biomedicines 10, n.º 8 (22 de julho de 2022): 1775. http://dx.doi.org/10.3390/biomedicines10081775.
Texto completo da fonteUrnovitz, H. B., e W. H. Murphy. "Human endogenous retroviruses: nature, occurrence, and clinical implications in human disease." Clinical Microbiology Reviews 9, n.º 1 (janeiro de 1996): 72–99. http://dx.doi.org/10.1128/cmr.9.1.72.
Texto completo da fonteEvdokimov, A. A., N. A. Mazurkova, E. G. Malygin, V. F. Zarytova, A. S. Levina, M. N. Repkova, S. N. Zagrebelnyi e N. A. Netesova. "Design of deoxyribozymes for inhibition of influenza a virus reproduction". Molecular Biology 47, n.º 1 (janeiro de 2013): 75–84. http://dx.doi.org/10.1134/s0026893312060040.
Texto completo da fonteKabanov, A. V., A. V. Ovcharenko, N. S. Melik-Hubarov, A. I. Bannikov, V. Yu Alakhov, V. I. Kiselev, P. G. Sveshnikov, O. I. Kiselev, A. V. Levashov e E. S. Severin. "Fatty acid acylated antibodies against virus suppress its reproduction in cells". FEBS Letters 250, n.º 2 (3 de julho de 1989): 238–40. http://dx.doi.org/10.1016/0014-5793(89)80729-x.
Texto completo da fonteTeses / dissertações sobre o assunto "Virus – Reproduction (biologie)"
Masante, Cyril. "Les minigénomes : un nouveau modèle de la réplication du VHC : mise en place et applications". Bordeaux 2, 2007. http://www.theses.fr/2007BOR21455.
Texto completo da fonteThe hepatitis C virus (HCV) affects around 170 million people worldwide and 3-4 million persons are infected each year. This infection will lead to death in 5-7 % of patients infected with HCV as a consequence of liver disease. The virus was first identified by Choo et al. (1989) but until recently development of new treatment for this infection has been hampered by the lack of an efficient cellular system. We established a new model to study HCV replication. In this system, the genes coding for the HCV non structural proteins are introduced in Huh7 cells (human hepatoma cell line) in order to constitutively express the HCV complex. Its activity is analysed by transfection of non-coding RNA (RNA minigenome) in the modified Huh7 cells. Those RNAs include EGFP and hygromycine genes surrounded by 5'UTR HCV non coding sequences. Those regions are included in order to be recognised by the HCV complex. The actvity of the HCV replication complex was determined by flow cytometry. Only cells able to support RNA minigenome replication could express the EGFP gene. RNA minigenome replication was detected in cells and could be maintained under hygromycine selection. I used this model to analyze the differences in replication activities between HCV genotype 1 and 3. We have identified 7 non contiguous nucleotides specific of genotype 3 in the 5'UTR, and those nucleotides are only present in this genotype, I showed these changes could be responsible for the reduced efficiency of RNA replication in the genotype 3. I also used this model to study the role of a cis-acting replication element, previously shown to be critical for the virus' replication. We have shown that this sequence is not required for the replication of our minigenome. I designed experiments to understand and explain the differences observed
Harrus, Déborah. "Compréhension des déterminants moléculaires de l'activation de la réplication du virus de l'hépatite C par corrélation d'informations biochimiques et structurales sur sa polymérase NS5B". Paris 11, 2010. http://www.theses.fr/2010PA114861.
Texto completo da fonteHepatitis C virus (HCV) is a highly varaible virus, classified in genotypes that differ in their geographical distribution, the seriousness of the liver disease they cause, and response et the available treatment. RNA-dependant RNA polymerase NS5B is a choice target for specific inhibitors of HCV. Its organization can be described as a catalytic domain comprising the 530 N-terminal residues connected by a 40-residue linker to a C-terminal 21-residue transmembrane anchor. The linker occludes the catalytic cleft in the crystal structures of NS5B, a conformation likely conducive to initiation of RNA synthesis but clearly inhibitory to elongation, both because of direct steric hindrance and because it locks NS5B in a closed conformation. The main objective of our research was the understanding of the molecular mechanisms of de novo RNA synthesis by HCV, and more specially the conformation changes that occurs during the transition between the initiation and the elongation steps. We proposed a diagram explaining the sequence of events alllowing RNA synthesis. It begins with NS5B's recognition of the viral genome, followed by the fixation of the first two incorporated nucleotides, and so this neo-synthesized dinucleotide repositioning thanks to NS5B's conformational changes to allow the further RNA elongation. This mechanism description highly improves our understanding of HCV-NS5B
Jakubiec, Anna. "Etude du complexe de réplication du virus de la mosaïque jaune du navet (TYMV) : assemblage et régulation". Paris 7, 2006. http://www.theses.fr/2006PA077111.
Texto completo da fonteTurnip yellow mosaic virus (TYMV) has a positive-stranded RNA genome encoding three proteins, one of which - the 206K -is essential for viral replication. In vitro and in vivo studies have revealed that the 206K is cleaved into two products: the 140K containing domains indicative of methyltransferase (MT), proteinase (PRO) and helicase (HEL) activities and the 66K encompassing RNA-dependent RNA polymerase. During my PhD I studied interactions between these proteins and determinants of their subcellular localisation in order to gain insight into molecular mechanisms underlying the assembly of viral replication complexes. This work supports a model wherein the 66K is recruited to the replication sites through an interaction with the PRO domain of the 140K, which is the membrane tether for viral replication complexes. Using antisera directed against different domains of the 206K precursor, we showed that the 140K was further processed in vivo into two products: 92K, containing the MT and PRO domains and 42K encompassing the HEL domain. Preliminary results indicate that the cleavage is not essential, but it is required for efficient viral replication. Eventually, we showed that the 66K polymerase was phosphorylated in vivo and several phosphorylated residues were identified by mass spectrometry analysis. Site directed mutagenesis experiments suggest two distinct functions for the 66K phosphorylation. We propose that phosphorylation in the N-terminal PEST sequence controls the metabolic stability of the 66K polymerase, while phosphorylation of its catalytic domain is involved in the regulation of viral RNA synthesis in the course of viral infection
Germon, Stéphanie. "Utilisation du modèle de l'hépatite B du canard pour la détermination de l'activité antivirale du L-FMAU et l'étude de la biologie de mutants de résistance à la lamivudine". Lyon 1, 1999. http://www.theses.fr/1999LYO1T274.
Texto completo da fonteLangon, Tania. "Clonage, séquençage et caractérisation des propriétés biologiques d'une souche très pathogène du virus de l'hépatite delta". Lyon 1, 1997. http://www.theses.fr/1997LYO1T288.
Texto completo da fonteLavedrine, Aude. "Caractérisation des protéines cellulaires sélectivement ciblées vers l’autophagie lors de l'infection par le virus de la rougeole". Electronic Thesis or Diss., Lyon 1, 2024. http://www.theses.fr/2024LYO10227.
Texto completo da fonteAutophagy is a highly conserved lysosomal catabolic process in eukaryotic cells that allows the degradation of a wide range of cytosolic components. This mechanism is essential for maintaining cellular homeostasis, particularly during invasions by intracellular pathogens. In this context, autophagy, referred to as xenophagy, serves as a key tool to defend the cell and eliminate the invader. However, many infectious agents have developed strategies to escape autophagic degradation or even hijack this process to their advantage. Our team has identified that the measles virus induces a complete autophagic process that contributes to enhancing viral replication. To understand how the measles virus manipulates autophagy, the objective of this thesis was to identify the nature of the cellular proteins degraded by this process during infection. In a first study, we demonstrated that two autophagy receptors, p62/SQSTM1 and TAX1BP1/T6BP, are degraded by virus-induced autophagy. The degradation of these two proteins impacts the intracellular cycle of bacteria co-infecting the cells, thus demonstrating the major influence of autophagy modulation by an infectious agent on cellular biology. To delve deeper, we then used a large-scale unbiased approach to identify the entire cellular proteome targeted within autophagosomes during measles virus infection. Beyond the 1031 proteins identified in the autophagosomes of infected cells, proteomic analysis and Gene Ontology highlighted a pro-viral factor, ILF3, which appears to inhibit the autophagic process during measles virus infection. Many other cellular pathways targeted toward autophagy during infection were also identified. This work paves the way for a better understanding of the complex interplay between autophagy and the measles virus, and more broadly, between autophagy and infectious microorganisms
Mateo, Mathieu. "Etude du rôle de la protéine VP24 dans la réplication , la pathogénicité et l'adaptation du virus Ebola". Lyon, Ecole normale supérieure, 2010. http://www.theses.fr/2010ENSL0611.
Texto completo da fonteThis PhD work highlight the critical role of the Ebola virus VP24 protein in the development of fatal hemorrhagic fevers associated with Ebola virus infections. Indeed, we have demonstrated that the acquisition of Ebola virus pathogenicity in the guinea-pig model is associated with modifications in the VP24 protein. We have identified two domains in VP24 which allow the virus to control the innate immune system and we have demonstrated that the adaptative mutations do not affect the IFN-antagonist function of VP24. Adaptative modifications in VP24 lead to a reduced interaction with the cellular KPNA1 protein and to a better interaction with viral components, allowing the proper assembly of infectious virus particles in the primary intected cells. We also identified a new function for VP24 in the control of the oxidative stress response
Nicot, Christophe. "Clonage d'un provirus infectieux du HTLV-1 : étude de la replication virale in vitro dans des types cellulaires de différentes origines". Bordeaux 2, 1995. http://www.theses.fr/1995BOR28342.
Texto completo da fonteReuse, Sophie. "Etude de la réactivation de l'expression des provirus HIV-1 latents par la prostratine en synergie avec des inhibiteurs de désacétylases: mécanismes moléculaires impliqués et potentiel thérapeutique". Doctoral thesis, Universite Libre de Bruxelles, 2009. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210213.
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Doctorat en Sciences
info:eu-repo/semantics/nonPublished
Etienne, Loïc. "Assemblage et sécrétion du virus de l'hépatite C : identification de dix résidus de la protéïne de capside importants pour optimiser la production du virus in vitro". Thesis, Tours, 2014. http://www.theses.fr/2014TOUR3309/document.
Texto completo da fonteDevelopment and cloning in 2005 of the highly replicative strain JFH-1 was a great opportunity to study the different stages of the infectious cycle of HCV as this strain easily propagate in the hepatocellular carcinoma cell line. Until now, these lates phases of particles assembly remain poorly understood, although the core protein is thought to probably play a major role in initiation of these mechanisms. Comparative studies of the capsid sequences of different strains of hepatitis C have allowed us to identify 10 specific residues in the JFH-1 strain that could explain the functional deficits of this protein. Indeed, the replacement in JFH-1 strain of these 10 residues by those most commonly found in strains of genotype 1 and 2 showed improvement of the assembly and secretion of new infectious particles and new subcellular localization of core. In addition, replacement of these ten residues by most common amino acid found in patients show a great enhancement of in vitro virus production and secretion. As a perspective, development of this optimized virus could also represent a valuable model to better purify and determine viral structure, and true viral assembly site; HCV fields that remain till now largely unknown
Livros sobre o assunto "Virus – Reproduction (biologie)"
NATO Advanced Study Institute Summer School on the Molecular Basis of Viral Replication (1986 Maratea, Italy). The molecular basis of viral replication. New York: Plenum Press, 1987.
Encontre o texto completo da fonteBercoff, R. The Molecular Basis of Viral Replication. Springer, 2013.
Encontre o texto completo da fonteBercoff, R. Molecular Basis of Viral Replication. Springer London, Limited, 2012.
Encontre o texto completo da fonteForeign DNA in mammalian systems. Weinheim: Wiley-VCH, 2000.
Encontre o texto completo da fonteCapítulos de livros sobre o assunto "Virus – Reproduction (biologie)"
Han, Mingyuan, Hanzhong Ke, Yijun Du, Qingzhan Zhang e Dongwan Yoo. "Reverse Genetics for Porcine Reproductive and Respiratory Syndrome Virus". In Methods in Molecular Biology, 29–46. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6964-7_3.
Texto completo da fonteNelson, E. A., J. Christopher-Hennings e D. A. Benfield. "Structural Proteins of Porcine Reproductive and Respiratory Syndrome Virus (PRRSV)". In Advances in Experimental Medicine and Biology, 321–23. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1899-0_52.
Texto completo da fonteUtsumi, Kenjiro, Yutaka Yokota, Takashi Ishikawa, Kunio Ohnishi e Kosaku Fujiwara. "Reproductive Disorders in Female SHR Rats Infected with Sialodacryoadenitis Virus". In Advances in Experimental Medicine and Biology, 525–32. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5823-7_73.
Texto completo da fonteMeulenberg, J. J. M., J. N. A. Bos-de Ruijter, G. Wensvoort e R. J. M. Moormann. "An Infectious cDNA Clone of Porcine Reproductive and Respiratory Syndrome Virus". In Advances in Experimental Medicine and Biology, 199–206. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5331-1_24.
Texto completo da fonteFaaberg, Kay S., Jun Han e Yue Wang. "Molecular Dissection of Porcine Reproductive and Respiratory Virus Putative Nonstructural Protein 2". In Advances in Experimental Medicine and Biology, 73–77. Boston, MA: Springer US, 2006. http://dx.doi.org/10.1007/978-0-387-33012-9_11.
Texto completo da fonteYoo, Dongwan, e Sarah Wootton. "Homotypic Interactions of the Nucleocapsid Protein of Porcine Reproductive and Respiratory Syndrome Virus (PRRSV)". In Advances in Experimental Medicine and Biology, 627–32. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1325-4_93.
Texto completo da fonteMagar, R., Y. Robinson, C. Dubuc e R. Larochelle. "Isolation and Experimental Oral Transmission in Pigs of a Porcine Reproductive and Respiratory Syndrome Virus Isolate". In Advances in Experimental Medicine and Biology, 139–44. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1899-0_23.
Texto completo da fonteMardassi, H., S. Mounir e S. Dea. "Structural Gene Analysis of a Quebec Reference Strain of Porcine Reproductive and Respiratory Syndrome Virus (PRRSV)". In Advances in Experimental Medicine and Biology, 277–81. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1899-0_44.
Texto completo da fonteMounir, S., H. Mardassi e S. Dea. "Identification and Characterization of the Porcine Reproductive and Respiratory Virus ORFS 7, 5 and 4 Products". In Advances in Experimental Medicine and Biology, 317–20. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1899-0_51.
Texto completo da fonteVanderheijden, N., P. Delputte, H. Nauwynck e M. Pensaert. "Effects of Heparin on the Entry of Porcine Reproductive and Respiratory Syndrome Virus into Alveolar Macrophages". In Advances in Experimental Medicine and Biology, 683–89. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1325-4_101.
Texto completo da fonteRelatórios de organizações sobre o assunto "Virus – Reproduction (biologie)"
Gottlieb, Yuval, Bradley Mullens e Richard Stouthamer. investigation of the role of bacterial symbionts in regulating the biology and vector competence of Culicoides vectors of animal viruses. United States Department of Agriculture, junho de 2015. http://dx.doi.org/10.32747/2015.7699865.bard.
Texto completo da fonteZchori-Fein, Einat, Judith K. Brown e Nurit Katzir. Biocomplexity and Selective modulation of whitefly symbiotic composition. United States Department of Agriculture, junho de 2006. http://dx.doi.org/10.32747/2006.7591733.bard.
Texto completo da fonteGottlieb, Yuval, e Bradley A. Mullens. Might Bacterial Symbionts Influence Vectorial Capacity of Biting Midges for Ruminant Viruses? United States Department of Agriculture, setembro de 2010. http://dx.doi.org/10.32747/2010.7699837.bard.
Texto completo da fonte