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Auswahl der wissenschaftlichen Literatur zum Thema „Virus – Reproduction (biologie)“
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Zeitschriftenartikel zum Thema "Virus – Reproduction (biologie)"
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Kennedy, Anissa, Jacob Herman und 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, Nr. 1823 (08.03.2021): 20190737. http://dx.doi.org/10.1098/rstb.2019.0737.
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Social insect reproductives exhibit exceptional longevity instead of the classic trade-off between somatic maintenance and reproduction. Even normally sterile workers experience a significant increase in life expectancy when they assume a reproductive role. The mechanisms that enable the positive relation between the antagonistic demands of reproduction and somatic maintenance are unclear. To isolate the effect of reproductive activation, honeybee workers were induced to activate their ovaries. These reproductively activated workers were compared to controls for survival and gene expression patterns after exposure to Israeli Acute Paralysis Virus or the oxidative stressor paraquat. Reproductive activation increased survival, indicating better immunity and oxidative stress resistance. After qPCR analysis confirmed our experimental treatments at the physiological level, whole transcriptome analysis revealed that paraquat treatment significantly changed the expression of 1277 genes in the control workers but only two genes in reproductively activated workers, indicating that reproductive activation preemptively protects against oxidative stress. Significant overlap between genes that were upregulated by reproductive activation and in response to paraquat included prominent members of signalling pathways and anti-oxidants known to affect ageing. Thus, while our results confirm a central role of vitellogenin, they also point to other mechanisms to explain the molecular basis of the lack of a cost of reproduction and the exceptional longevity of social insect reproductives. Thus, socially induced reproductive activation preemptively protects honeybee workers against stressors, explaining their longevity. This article is part of the theme issue ‘Ageing and sociality: why, when and how does sociality change ageing patterns?'
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Uddin, Mohammed Nizam, Sofi Mahmud Parvez, H. M. Shahadat Ali, Muhammad Samsuddin und 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, Nr. 2 (18.06.2022): 469–76. http://dx.doi.org/10.31018/jans.v14i2.3398.
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In the middle of December 2019, a virus known as coronavirus (COVID-19) generated by severe acute respiratory syndrome corona virus 2 (SARC-CoV-2) was first detected in Wuhan, Hubei Province, China. As of the 9th of March, 2022, spread to over 212 countries, causing 429 million confirmed cases and 6 million people to lose their lives worldwide. In developing countries like the South Asian area, alarming dynamic variations in the pattern of confirmed cases and death tolls were displayed. During epidemics, accurate assessment of the characteristics that characterize infectious disease transmission is critical for optimizing control actions, planning, and adapting public health interventions. The reproductive number, or the typical number of secondary cases caused by an infected individual, can be employed to determine transmissibility. Several statistical and mathematical techniques have been presented to calculate across the duration of an epidemic. A technique is provided for calculating epidemic reproduction numbers. It is a MATLAB version of the EpiEstim package's R function estimate R, version 2.2-3. in the South Asian Association for Regional Cooperation (SAARC) countries. The three methodologies supported are 'parametric SI,' 'non-parametric SI,' and 'uncertain SI.' The present study indicated that the highest reproduction number was 12.123 and 11.861 on 5th and 14th March 2020 in India and Sri_Lanka, whereas the lowest reproduction number was the lowest was 0.300 and 0.315 in Sri_Lanka and India. The Maximum and minimum reproductive number of Bangladesh was 3.752 and 0.725. In this study, we have tried to point out the worst, best and current situation of SAARC countries.
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G, Gulothungan, Vickram A S und 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, Nr. 5 (31.10.2022): 960–77. http://dx.doi.org/10.18006/2022.10(5).960.977.
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Coronavirus disease 2019 (COVID 19) is caused by severe acute respiratory syndrome novel coronavirus 2 (SARS-nCoV-2). It has been declared a pandemic by the World Health Organization (WHO) on March 11, 2020. Since then, several researchers have worked/ are working on this virus by a multifactorial approach to finding out the mechanism of entry, transmission route, post-infection replication process, survival, and post-recovery utilities. As we know, SARS, MERS, and Zika viruses have affected human reproductive potentials, consequently, COVID 19 also can affect both men's and women's reproductive potential through ACE2 macromolecule. This study aimed to summarize the role of ACE2- macromolecule in COVID 19 entry and further processes in the reproductive path of both men and women. Research articles were searched in NCBI-NLM, Google Scholar, and Scopus databases. We searched based on the phrase “COVID 19”, “ACE2”, “ACE2 in testes”, “ACE2 in the female reproductive tract”, “ACE2 during pregnancy”, “ACE2 during early embryo”, “COVID 19 and impact in human reproduction” and selected the articles for summarizing this article. Most recent articles and the mechanism of COVID 19 were selected for our understanding. The results of the study revealed that COVID 19 impacts the reproductive potential of both men and women. Testes are the most vulnerable organ prone to infection in men, and vaginal fluid and the uterus could be the choice of infection in the female. Till now, COVID 19 has not been directly detected in semen samples and vaginal fluid. Results of the study can be concluded that ACE2 plays a major role in COVID 19 infection, ACE2 expression could be more in the testes, ovary, uterus, and vagina. COVID 19 could impact more on human reproduction and lead to a loss of fertility status for a while. All antiviral treatments could pose a negative impact on human reproduction. Further research should be carried out on the already existing theoretical hypothesis of SARS-Co-V-2 on human reproduction.
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MANDELBROT, LAURENT, und ROGER HENRION. „Human Immunodeficiency Virus and Reproduction“. Annals of the New York Academy of Sciences 626, Nr. 1 Frontiers in (Juni 1991): 484–501. http://dx.doi.org/10.1111/j.1749-6632.1991.tb37941.x.
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Valansi, Clari, David Moi, Evgenia Leikina, Elena Matveev, Martín Graña, Leonid V. Chernomordik, Héctor Romero, Pablo S. Aguilar und Benjamin Podbilewicz. „Arabidopsis HAP2/GCS1 is a gamete fusion protein homologous to somatic and viral fusogens“. Journal of Cell Biology 216, Nr. 3 (30.01.2017): 571–81. http://dx.doi.org/10.1083/jcb.201610093.
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Cell–cell fusion is inherent to sexual reproduction. Loss of HAPLESS 2/GENERATIVE CELL SPECIFIC 1 (HAP2/GCS1) proteins results in gamete fusion failure in diverse organisms, but their exact role is unclear. In this study, we show that Arabidopsis thaliana HAP2/GCS1 is sufficient to promote mammalian cell–cell fusion. Hemifusion and complete fusion depend on HAP2/GCS1 presence in both fusing cells. Furthermore, expression of HAP2 on the surface of pseudotyped vesicular stomatitis virus results in homotypic virus–cell fusion. We demonstrate that the Caenorhabditis elegans Epithelial Fusion Failure 1 (EFF-1) somatic cell fusogen can replace HAP2/GCS1 in one of the fusing membranes, indicating that HAP2/GCS1 and EFF-1 share a similar fusion mechanism. Structural modeling of the HAP2/GCS1 protein family predicts that they are homologous to EFF-1 and viral class II fusion proteins (e.g., Zika virus). We name this superfamily Fusexins: fusion proteins essential for sexual reproduction and exoplasmic merger of plasma membranes. We suggest a common origin and evolution of sexual reproduction, enveloped virus entry into cells, and somatic cell fusion.
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Rybalko, 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, Nr. 1 (31.03.2001): 241–49. http://dx.doi.org/10.18388/abp.2001_5132.
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Copolymers of N-polyvinylpyrrolidone-acrylic acid (AB-1) and adamantane derivatives are known to possess marked antiviral activity in in vitro and in ovo models. Among the constructed preparations of AB-1 modified by adamantane derivatives some, especially AB-4 (modified by deitiforin), were found to show more extended antiviral activity and to inhibit markedly virus reproduction in susceptible permissive cell cultures and chicken embryos. In AB-4 treated cells and allantoic sacs, virus titers (influenza virus, herpes virus, and HIV) and virus antigen concentration were decreased. On the other hand, herpes virus-specific thymidine kinase and of DNA-polymerases isolated from Escherichia coli, Plectonema boryanum, and herpes virus type 1 infected murine brain tissue retained their activity after incubation with AB-4 or AB-2. The compounds investigated, in view of their effect on virus reproduction, are thought to be prospective as antiviral agents.
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Harb, Julien, Nour Debs, Mohamad Rima, Yingliang Wu, Zhijian Cao, Hervé Kovacic, Ziad Fajloun und Jean-Marc Sabatier. „SARS-CoV-2, COVID-19, and Reproduction: Effects on Fertility, Pregnancy, and Neonatal Life“. Biomedicines 10, Nr. 8 (22.07.2022): 1775. http://dx.doi.org/10.3390/biomedicines10081775.
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Since its discovery in Wuhan, China, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has spread over the world, having a huge impact on people’s lives and health. The respiratory system is often targeted in people with the coronavirus disease 2019 (COVID-19). The virus can also infect many organs and tissues in the body, including the reproductive system. The consequences of the SARS-CoV-2 infection on fertility and pregnancy in hosts are poorly documented. Available data on other coronaviruses, such as severe acute respiratory syndrome (SARS-CoV) and Middle Eastern Respiratory Syndrome (MERS-CoV) coronaviruses, identified pregnant women as a vulnerable group with increased pregnancy-related complications. COVID-19 was also shown to impact pregnancy, which can be seen in either the mother or the fetus. Pregnant women more likely require COVID-19 intensive care treatment than non-pregnant women, and they are susceptible to giving birth prematurely and having their newborns admitted to the neonatal intensive care unit. Angiotensin converting enzyme 2 (ACE2), a key player of the ubiquitous renin-angiotensin system (RAS), is the principal host cellular receptor for SARS-CoV-2 spike protein. ACE2 is involved in the regulation of both male and female reproductive systems, suggesting that SARS-CoV-2 infection and associated RAS dysfunction could affect reproduction. Herein, we review the current knowledge about COVID-19 consequences on male and female fertility, pregnant women, and their fetuses. Furthermore, we describe the effects of COVID-19 vaccination on reproduction.
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Urnovitz, H. B., und W. H. Murphy. „Human endogenous retroviruses: nature, occurrence, and clinical implications in human disease.“ Clinical Microbiology Reviews 9, Nr. 1 (Januar 1996): 72–99. http://dx.doi.org/10.1128/cmr.9.1.72.
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Retroviral diagnostics have become standard in human laboratory medicine. While current emphasis is placed on the human exogenous viruses (human immunodeficiency virus and human T-cell leukemia virus), evidence implicating human endogenous retroviruses (HERVs) in various human disease entities continues to mount. Literature on the occurrence of HERVs in human tissues and cells was analyzed. Substantial evidence documents that retrovirus particles were clearly demonstrable in various tissues and cells in both health and disease and were abundant in the placenta and that their occurrence could be implicated in some of the reproductive diseases. The characteristics of HERVs are summarized, mechanisms of replication and regulation are outlined, and the consistent hormonal responsiveness of HERVs is noted. Clear evidence implicating HERV gene products as participants in glomerulonephritis in some cases of systemic lupus erythematosus is adduced. Data implicating HERVs as etiologic factors in reproductive diseases, in some of the autoimmune diseases, in some forms of rheumatoid arthritis and connective tissue disease, in psoriasis, and in some of the inflammatory neurologic diseases are reviewed. The current major needs are to improve methods for HERV detection, to identify the most appropriate HERV prototypes, and to develop diagnostic reagents so that the putative biologic and pathologic roles of HERVs can be better evaluated.
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Evdokimov, A. A., N. A. Mazurkova, E. G. Malygin, V. F. Zarytova, A. S. Levina, M. N. Repkova, S. N. Zagrebelnyi und N. A. Netesova. „Design of deoxyribozymes for inhibition of influenza a virus reproduction“. Molecular Biology 47, Nr. 1 (Januar 2013): 75–84. http://dx.doi.org/10.1134/s0026893312060040.
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Kabanov, 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 und E. S. Severin. „Fatty acid acylated antibodies against virus suppress its reproduction in cells“. FEBS Letters 250, Nr. 2 (03.07.1989): 238–40. http://dx.doi.org/10.1016/0014-5793(89)80729-x.
Der volle Inhalt der QuelleDissertationen zum Thema "Virus – Reproduction (biologie)"
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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.
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Le virus de l'hépatite C (VHC) affecte 170 millions de personnes dans le monde. Quatre-vingt pour cent des individus atteints vont développer une hépatite chronique voire une cirrhose puis un cancer du foie pour certains d'entre eux. Il n'existe actuellement qu'un seul traitement contre le virus, mais il n'est efficace que pour la moitié des patients. Notre projet consiste à mieux comprendre les mécanismes de réplication du virus dans le but de développer de nouveaux inhibiteurs. Au cours de ma thèse j'ai participé au développement d'un nouveau modèle de la réplication du VHC. Ce modèle cellulaire permet une étude dissociée des deux principales activités virales, ce qui est actuellement impossible avec les autres modèles utilisés. Pour cela, les protéines virales nécessaires à la réplication sont constamment produites dans des cellules. Elles s'associent en un complexe qui va répliquer une molécule d'acide nucléique contenant un gène rapporteur encadré par les séquences de reconnaissance virale. Cette molécule perpétuellement dupliquée à chaque cycle, révèle un mécanisme de réplication proche de celui utilisé par le virus. Ce modèle de la réplication du VHC a déjà permis de mettre en évidence une diminution de l'activité réplicative chez les virus de génotype 3. Sept variations nucléotidiques situées dans une région du génome viral impliquée dans la traduction et la réplication du virus en sont responsables. Cette spécificité de séquence pourrait ainsi expliquer la meilleure réponse au traitement par l'interféron observée chez les patients infectés par les virus de génotype 3. D'autre part, nous avons montré que les molécules répliquées dans ce système sont dépourvues d'une structure réputée indispensable à la synthèse du génome viral. Cette structure appelée 5BSL3. 2 est néanmoins indispensable à la prolifération du virus. La deuxième partie de mon projet de thèse a donc consisté à caractériser la 5BSL3. 2 et plus particulièrement à analyser son rôle dans la traduction des protéines viralesThe 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
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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.
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Le virus de l'hépatite C (VHC) est un virus variable classifié en génotypes, qui diffèrent par leur distribution géographique, la sévérité des dommages causés au foie, et leur réponse aux traitements. L'ARN polymérase dépendante de l'ARN NS5B est une cible de choix pour les inhibiteurs du VHC. Les structures cristallographiques décrivent son organisation en 3 domaines appelés "doigts", "paume" et "pouce", le site catalytique se situant à la jonction entre ces trois domaines. Un segment C-Terminal de 40 acides aminés appelé "connecteur" part du pouce et relie les 530 résidus N-terminaux à une ancre transmembranaire de 21 résidus. La position du connecteur, replié au sein de la crevasse catalytique, est critique pour l'initiation de la synthèse d'ARN mais inhibitrice pour le processus d'élongation puisqu'il bloque l'enzyme en forme "pouce fermé". L'objectif de ce travail a été de réunir des informations biochimiques et structurales sur NS5B afin de mieux comprendre les mécanismes de la synthèse d'ARN de novo par le VHC, et plus spécifiquement les changements de conformation qui ont lieu lors de la transition entre les étapes d'initiation de d'élongation. Nous proposons un schéma explicatif de la séquence d'événements qui permettent la synthèse d'ARN. Celle-ci débute par la reconnaissance et la fixation de NS5B sur le génome viral, suivi par la fixation des deux premiers nucléotides incorporés, puis un repositionnement du dinucléotide néo-synthétisé grâce à des changements de conformation de NS5B pour permettre la poursuite de la synthèse d'ARN. La description de ce mécanisme constitue une avancée importante dans la compréhension du fonctionnement de VHC-NS5BHepatitis 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
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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.
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Le virus de la mosaïque jaune du navet (ou TYMV) possède un génome constitué d'ARN de polarité positive. Il code trois protéines, dont une - la 206K - est essentielle à la replication virale. Des études in vitro et in vivo ont permis de montrer que cette protéine subit un clivage générant les produits 140K, contenant les domaines méthyltransférase (MT), protéase (PRO) et hélicase (HEL), et 66K, qui correspond à l'ARN polymérase ARN-dépendante (POL). Au cours de ma thèse j'ai étudié les interactions entre ces protéines et le déterminisme de leur adressage subcellulaire dans le but de mieux comprendre le processus d'assemblage des complexes de replication. Ces travaux ont abouti à un modèle selon lequel la 66K est recrutée dans les complexes de replication par le biais de son interaction avec le domaine PRO de la 140K, portant les déterminants d'adressage aux membranes cibles. A l'aide d'antiséra spécifiques de différents domaines du précurseur 206K nous avons pu montrer que la 140K subit in vivo au moins un clivage supplémentaire, qui donne lieu à la formation deux produits : 92K, portant les domaines MT et PRO, et 42K qui correspond au domaine HEL. Des résultats préliminaires indiquent que ce clivage n'est pas essentiel à la replication, mais qu'il contribue à son efficacité. Finalement, nous avons pu montrer que la polymérase 66K est phosphorylée in vivo et les sites de phosphorylation ont pu être caractérisés. La phosphorylation aurait au moins deux fonctions au cours du cycle viral : elle serait impliquée dans le contrôle de la stabilité de la polymérase et dans la régulation de l'équilibre entre les différents types d'ARN viraux synthétisés au cours du cycle viralTurnip 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
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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.
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Langon, 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.
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Lavedrine, 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.
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L’autophagie est un processus du catabolisme lysosomal hautement conservé dans les cellules eucaryotes, permettant la dégradation d’un large spectre de composants cytosoliques. Ce mécanisme est essentiel au maintien de l’homéostasie cellulaire, notamment lors d’invasions par des pathogènes intracellulaires. Dans ce contexte, l’autophagie, désignée sous le terme de xénophagie, constitue un outil clé pour défendre la cellule et éliminer l’envahisseur. Cependant, de nombreux agents infectieux ont développé des stratégies pour échapper à la dégradation autophagique, voire pour détourner ce processus à leur avantage. Notre équipe a identifié que le virus de la rougeole induit un processus autophagique complet qui contribue à favoriser la réplication virale. Afin de comprendre comment le virus de la rougeole manipule l’autophagie, l’objectif de ce travail de thèse a été d’identifier la nature des protéines cellulaires dégradées par ce processus lors de l’infection. Dans une première étude, nous avons montré que deux récepteurs autophagiques, p62/SQSTM1 et TAX1BP1/T6BP, sont dégradés par l’autophagie viro-induite. La dégradation de ces deux protéines impacte le cycle intracellulaire de bactéries co-infectants les cellules, démontrant ainsi l’influence majeure de la modulation de l’autophagie par un agent infectieux sur la biologie de la cellule. Afin d’aller plus loin, nous avons ensuite utilisé une approche à large échelle non biaisée pour identifier l’ensemble du protéome cellulaire ciblé dans les autophagosomes lors de l’infection par le virus de la rougeole. Au-delà des 1031 protéines identifiées dans les autophagosomes des cellules infectées, l’étude protéomique et son analyse par Gene Ontology ont permis de mettre en lumière un facteur pro-viral, ILF3, qui semble inhiber le processus autophagique lors de l’infection par le virus de la rougeole. De nombreuses autres voies cellulaires ciblées vers l’autophagie lors de l’infection ont également été identifiées. Ce travail ouvre la voie à une meilleure compréhension de la relation complexe entre l’autophagie et le virus de la rougeole, et, de manière plus générale, entre l’autophagie et les micro-organismes infectieuxAutophagy 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
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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.
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Ces travaux de thèses mettent en évidence le rôle critique de la protéine VP24 du virus Ebola dans le développement des fièvres hémorragiques mortelles associées à l'infection par ce virus. En effet, nous avons démontré que l'acquisition de la pathogénicité du virus Ebola dans le modèle cobaye est associée à des changements de la protéine VP24. Nous avons identifié des domaines protéiques de VP24 qui permettent au virus de contrôler la réponse immunitaire innée et nous avons démontré que les mutations adaptatives n'affectent pas la fonction IFN-antagoniste de la protéine VP24. Les changements adaptatifs de la protéine VP24 ont pour effet de réduire son interaction avec la protéine cellulaire KPNA1 et d'améliorer son interaction avec les composants viraux afin d'assurer la formation de particules virales infectieuses dans les cellules primo-infectées. Nous avons par ailleurs identifié une nouvelle fonction de la protéine VP24 dans le contrôle de la réponse au stress oxydatifThis 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
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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.
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Reuse, 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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L’infection par HIV-1 représente un des problèmes de santé publique majeurs de notre société actuelle. Le traitement HAART (Highly Active AntiRetroviral Therapy) inhibe le cycle réplicatif viral mais ne permet pas l’éradication du HIV-1. La principale cause de cet échec thérapeutique est la persistance de réservoirs cellulaires infectés de manière latente par HIV-1, qui, lors de l’arrêt du traitement HAART, sont à l’origine d’un rebond de la charge plasmatique virale. Le défi actuel est donc de découvrir de nouvelles méthodes d’élimination des cellules réservoirs. Une des stratégies envisagées est de forcer l’expression virale dans les cellules infectées de manière latente afin d’entraîner leur destruction suite à leur détection par le système immunitaire ou suite aux effets cytopathiques viraux. Parallèlement, le traitement HAART serait maintenu afin de limiter la propagation des virions néo-synthétisés. Plusieurs éléments sont impliqués dans la répression transcriptionnelle associée à la latence post-intégrationnelle du virus HIV-1 :la nature du site d’intégration ;l’absence de facteurs cellulaires inductibles tels que NF-κB ;la structure chromatinienne du provirus et les modifications post-traductionnelles des histones ;l’absence de niveaux suffisants de la protéine trans-activatrice Tat. De plus, notre laboratoire a précédemment mis en évidence un lien entre deux de ces éléments, en démontrant, dans une lignée modèle de latence post-intégrationnelle, que la cytokine pro-inflammatoire TNFα, un activateur de la voie de signalisation NF-κB, permet une réactivation synergique de l’expression virale combinée à l’inhibiteur d’histone-désacétylases (HDACI) TSA. Cependant, l’utilisation thérapeutique du TNFα et de la TSA est inenvisageable en raison de leurs toxicités.\
Doctorat en Sciences
info:eu-repo/semantics/nonPublished
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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.
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La mise au point en 2005 d’un modèle de propagation sur lignée d’hépatocarcinome basé sur la souche hautement réplicative JFH-1 fut une formidable opportunité d’étudier les différentes étapes du cycle infectieux du VHC. Nous avons souhaité étudier les étapes de morphogenèse et de sécrétion du virus, des phases du cycle viral qui sont largement mal connues encore aujourd’hui, mais ou la protéine de capside joue probablement un rôle majeur. Des études comparatives des séquences de capsides de différentes souches du VHC nous ont permis de mettre en évidence 10 résidus spécifiques à la souche JFH-1 qui pourraient expliquer les déficits fonctionnels connus de cette protéine. En effet, le remplacement de ces 10 résidus par ceux plus communément retrouvés dans les souches de génotype 1 et 2 a permis une amélioration significative de l’assemblage et de la sécrétion des particules infectieuses produites. La mise au point de cette souche optimisée pour la production de virus pourrait par ailleurs permettre constituer un atout pour mieux comprendre la structure du virus par des techniques de microscopie électronique ; ce type d’étude n’ayant pas pu être véritablement menée jusqu’à présent, en raison des titres infectieux insuffisants obtenus avec la souche JFH-1 sauvageDevelopment 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
Bücher zum Thema "Virus – Reproduction (biologie)"
1
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.
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2
Bercoff, R. The Molecular Basis of Viral Replication. Springer, 2013.
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3
Bercoff, R. Molecular Basis of Viral Replication. Springer London, Limited, 2012.
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4
Foreign DNA in mammalian systems. Weinheim: Wiley-VCH, 2000.
Den vollen Inhalt der Quelle findenBuchteile zum Thema "Virus – Reproduction (biologie)"
1
Han, Mingyuan, Hanzhong Ke, Yijun Du, Qingzhan Zhang und 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.
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2
Nelson, E. A., J. Christopher-Hennings und 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.
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3
Utsumi, Kenjiro, Yutaka Yokota, Takashi Ishikawa, Kunio Ohnishi und 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.
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4
Meulenberg, J. J. M., J. N. A. Bos-de Ruijter, G. Wensvoort und 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.
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Faaberg, Kay S., Jun Han und 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.
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Yoo, Dongwan, und 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.
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Magar, R., Y. Robinson, C. Dubuc und 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.
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Mardassi, H., S. Mounir und 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.
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Mounir, S., H. Mardassi und 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.
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Vanderheijden, N., P. Delputte, H. Nauwynck und 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.
Der volle Inhalt der QuelleBerichte der Organisationen zum Thema "Virus – Reproduction (biologie)"
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Gottlieb, Yuval, Bradley Mullens und 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, Juni 2015. http://dx.doi.org/10.32747/2015.7699865.bard.
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Symbiotic bacteria have been shown to influence host reproduction and defense against biotic and abiotic stressors, and this relates to possible development of a symbiont-based control strategy. This project was based on the hypothesis that symbionts have a significant impact on Culicoides fitness and vector competence for animal viruses. The original objectives in our proposal were: 1. Molecular identification and localization of the newly-discovered symbiotic bacteria within C. imicola and C. schultzei in Israel and C. sonorensis in California. 2. Determination of the prevalence of symbiotic bacteria within different vector Culicoides populations. 3. Documentation of specific symbiont effects on vector reproduction and defense: 3a) test for cytoplasmic incompatibility in Cardinium-infected species; 3b) experimentally evaluate the role of the symbiont on infection or parasitism by key Culicoides natural enemies (iridescent virus and mermithid nematode). 4. Testing the role(s) of the symbionts in possible protection against infection of vector Culicoides by BTV. According to preliminary findings and difficulties in performing experimental procedures performed in other insect symbiosis systems where insect host cultures are easily maintained, we modified the last two objectives as follows: Obj. 3, we tested how symbionts affected general fitness of Israeli Culicoides species, and thoroughly described and evaluated the correlation between American Culicoides and their bacterial communities in the field. We also tried alternative methods to test symbiont-Culicoides interactions and launched studies to characterize low-temperature stress tolerances of the main US vector, which may be related to symbionts. Obj. 4, we tested the correlation between EHDV (instead of BTV) aquisition and Cardinium infection. Culicoides-bornearboviral diseases are emerging or re-emerging worldwide, causing direct and indirect economic losses as well as reduction in animal welfare. One novel strategy to reduce insects’ vectorial capacity is by manipulating specific symbionts to affect vector fitness or performance of the disease agent within. Little was known on the bacterial tenants occupying various Culicoides species, and thus, this project was initiated with the above aims. During this project, we were able to describe the symbiont Cardinium and whole bacterial communities in Israeli and American Culicoides species respectively. We showed that Cardinium infection prevalence is determined by land surface temperature, and this may be important to the larval stage. We also showed no patent significant effect of Cardinium on adult fitness parameters. We showed that the bacterial community in C. sonorensis varies significantly with the host’s developmental stage, but it varies little across multiple wastewater pond environments. This may indicate some specific biological interactions and allowed us to describe a “core microbiome” for C. sonorensis. The final set of analyses that include habitat sample is currently done, in order to separate the more intimately-associated bacteria from those inhabiting the gut contents or cuticle surface (which also could be important). We were also able to carefully study other biological aspects of Culicoides and were able to discriminate two species in C. schultzei group in Israel, and to investigate low temperature tolerances of C. sonorensis that may be related to symbionts. Scientific implications include the establishment of bacterial identification and interactions in Culicoides (our work is cited in other bacteria-Culicoides studies), the development molecular identification of C. schultzei group, and the detailed description of the microbiome of the immature and matched adult stages of C. sonorensis. Agricultural implications include understanding of intrinsic factors that govern Culicoides biology and population regulation, which may be relevant for vector control or reduction in pathogen transmission. Being able to precisely identify Culicoides species is central to understanding Culicoides borne disease epidemiology.
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Zchori-Fein, Einat, Judith K. Brown und Nurit Katzir. Biocomplexity and Selective modulation of whitefly symbiotic composition. United States Department of Agriculture, Juni 2006. http://dx.doi.org/10.32747/2006.7591733.bard.
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Whiteflies are sap-sucking insects that harbor obligatory symbiotic bacteria to fulfill their dietary needs, as well as a facultative microbial community with diverse bacterial species. The sweetpotato whitefly Bemisia tabaci (Gennadius) is a severe agricultural pest in many parts of the world. This speciesconsists of several biotypes that have been distinguished largely on the basis of biochemical or molecular diagnostics, but whose biological significance is still unclear. The original objectives of the project were (i) to identify the specific complement of prokaryotic endosymbionts associated with select, well-studied, biologically and phylogeographically representative biotypes of B. tabaci, and (ii) to attempt to 'cure’ select biotypes of certain symbionts to permit assessment of the affect of curing on whitefly fitness, gene flow, host plant preference, and virus transmission competency.To identify the diversity of bacterial community associated with a suite of phylogeographically-diverseB. tabaci, a total of 107 populations were screened using general Bacteria primers for the 16S rRNA encoding gene in a PCR. Sequence comparisons with the available databases revealed the presence of bacteria classified in the: Proteobacteria (66%), Firmicutes (25.70%), Actinobacteria (3.7%), Chlamydiae (2.75%) and Bacteroidetes (<1%). Among previously identified bacteria, such as the primary symbiont Portiera aleyrodidarum, and the secondary symbionts Hamiltonella, Cardinium and Wolbachia, a Rickettsia sp. was detected for the first time in this insect family. The distribution, transmission, and localization of the Rickettsia were studied using PCR and fluorescence in situ hybridization (FISH). Rickettsia was found in all 20 Israeli B. tabaci populations screened as well as some populations screened in the Arizona laboratory, but not in all individuals within each population. FISH analysis of B. tabaci eggs, nymphs and adults, revealed a unique concentration of Rickettsia around the gut and follicle cells as well as its random distribution in the haemolymph, but absence from the primary symbiont housing cells, the bacteriocytes. Rickettsia vertical transmission on the one hand and its partial within-population infection on the other suggest a phenotype that is advantageous under certain conditions but may be deleterious enough to prevent fixation under others.To test for the possible involvement of Wolbachia and Cardiniumin the reproductive isolation of different B. tabacibiotypes, reciprocal crosses were preformed among populations of the Cardinium-infected, Wolbachia-infected and uninfected populations. The crosses results demonstrated that phylogeographically divergent B. tabaci are reproductively competent and that cytoplasmic incompatibility inducer-bacteria (Wolbachia and Cardinium) both interfered with, and/or rescued CI induced by one another, effectively facilitating bidirectional female offspring production in the latter scenario.This knowledge has implications to multitrophic interactions, gene flow, speciation, fitness, natural enemy interactions, and possibly, host preference and virus transmission. Although extensive and creative attempts undertaken in both laboratories to cure whiteflies of non-primary symbionts have failed, our finding of naturally uninfected individuals have permitted the establishment of Rickettsia-, Wolbachia- and Cardinium-freeB. tabaci lines, which are been employed to address various biological questions, including determining the role of these bacteria in whitefly host biology.
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Gottlieb, Yuval, und Bradley A. Mullens. Might Bacterial Symbionts Influence Vectorial Capacity of Biting Midges for Ruminant Viruses? United States Department of Agriculture, September 2010. http://dx.doi.org/10.32747/2010.7699837.bard.
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- Original objectives and revision: The feasibility study performed in the last year was aimed at determining the symbiotic profiles of eight selected Culicoidesspecies in Israel and the USA by: Comparing bacterial communities among geographic populations of primary bluetongue virus (BTV) vectors. Comparing bacterial communities between adults of field-collected, mammal-feeding BTV vectors and non-vectors. Comparing bacterial communities within and between mammal feeders and bird feeders, with special attention to species with unique immature habitats. We made an effort to collect the eight species during the beginning of the project, however, due to the short available collection season, and the significant changes in habitats available for Israeli Culicoides, we initially determined the symbiotic profile of five species: two BTV vectors (C. sonorensis, C. imicola), one mammal feeders with unknown vectoring ability (C. schultzei), one bird feeder (C. crepuscularis), and one unique habitat species (C. cacticola). In addition, upon preliminary symbiont identification we focused our effort on relevant specific symbionts. Background: Biting midges (Culicoides, Diptera: Ceratopogonidae) are vectors of many major viral diseases affecting farm animals, including BT, which is listed among the most damaging by the World Organization for Animal Health (OIE) and has recently emerged in completely unexpected areas (Northern Europe). One of the strategies to reduce the vectorial capacity of insect vectors is by manipulating their specific symbionts either to affect the vector species or to influence performance of the disease agent within it. Despite significant efforts to elucidate the vectorial capacity of certain Culicoidesspecies, and the critical basis of variability in infection, almost no attention has been given to symbiotic interactions between the vector and its bacterial tenants. It is now established that bacterial symbionts have major influences on their host biology, and may interact with disease agents vectored by their hosts. - Major conclusions, solutions, achievements: During the feasibility project we have found two major bacterial symbionts in Israeli and American Culicoides. In Israel we discovered that C. imicola, a known vector of BT, and C. schultzeigp. a suspected vector of BT, carry the symbiotic bacterium Cardinium, a reproductive manipulator symbiont. In C. imicolathe infection rate was close to 50%, and in C. schultzeiit was lower, and restricted to one of two species within Schultzeigroup. In 3 American species (C. sonorensis, C. crepuscularis, C. cacticola) we found the bacterium Burkholderiasp. In all species tested we have also found other bacterial species in diverse quantities and frequencies. - Implications, both scientific and agricultural: Finding specific symbionts in Culicoidesvector species is the first step in developing symbiont based control (SBC) strategies. Both identified symbionts are known from other insects, and Cardiniumis also known as a reproductive manipulator that can cause cytoplasmic incompatibility, an important phenomenon that can be used for spreading desired traits in infected populations. The role of the symbionts in Culicoideshost can be target for manipulation to reduce the vectorial capacity of the host by either changing its fitness so that it is unable to serve as a vector, or by directly changing the symbiont in a way that will affect the performance of the disease agent in its vector. Since Burkholderiaperhaps can be cultured independently of the host, it is a promising candidate for the later option. Thus, we have now opened the door for studying the specific interactions between symbionts and vector species.