Journal articles: 'Propagation virale'

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Morelli, Pierre. "L'Image au Défi de Sa Propagation Virale." مدارات, no. 29-30 (June 2017): 7–32. http://dx.doi.org/10.12816/0050243.

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Abeywickrama-Samarakoon, Natali, Jean-Claude Cortay, Camille Sureau, Dulce Alfaiate, Massimo Levrero, and Paul Dény. "Réplication du génome du virus de l’hépatite delta : un rôle pour la petite protéine delta S-HDAg." médecine/sciences 34, no. 10 (October 2018): 833–41. http://dx.doi.org/10.1051/medsci/2018209.

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Le virus de l’hépatite delta, aussi appelé virus de l’hépatite D ou HDV, est un agent viral défectif à ARN de polarité négative. Il se réplique dans les cellules de mammifère et infecte l’homme. Son génome est un petit ARN circulaire monocaténaire d’environ 1 680 nucléotides. Pour se propager, HDV a cependant besoin d’un autre virus, le virus de l’hépatite B (HBV), qui lui fournit les protéines d’enveloppe nécessaires à l’assemblage de ses virions et à la propagation de l’infection. Les manifestations cliniques graves de l’infection combinée HBV-HDV vont des formes aiguës d’hépatites fulminantes aux formes chroniques de fibroses du foie (cirrhose), qui peuvent conduire à un carcinome hépatocellulaire. Une originalité de l’HDV repose sur la ressemblance de son génome avec celui des viroïdes, des agents infectieux des plantes constitués de petits ARN circulaires non encapsidés. Dépourvu de toute activité réplicase virale, l’HDV doit utiliser l’activité ARN polymérase-ADN dépendante de la cellule qu’il infecte pour répliquer son ARN génomique. Comment dès lors, cette réplication se réalise ? Nous aborderons dans cette revue les principales étapes de la transcription et de la réplication de ces ARN viraux.

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Balasubramanian, Saravanakarthikeyan, and Divya Vinayachandran. "Bioaérosols provenant de la respiration buccale : mode de transmission méconnu de la COVID-19?" Relevé des maladies transmissibles au Canada 47, no. 56 (June 9, 2021): 302–5. http://dx.doi.org/10.14745/ccdr.v47i56a05f.

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Le monde entier a été touché par la pandémie de maladie à coronavirus 2019 (COVID-19), et de nombreux chercheurs se lancent dans une course pour comprendre l’évolution de la maladie et entreprendre des analyses de risque afin de formuler des stratégies de traitement efficaces. Le coronavirus du syndrome respiratoire aigu sévère 2 (SRAS-CoV-2) est très transmissible par la toux et les éternuements, ainsi que par la respiration et en parlant, ce qui peut expliquer la transmission virale à partir de porteurs asymptomatiques. Les bioaérosols produits pendant la respiration buccale, un processus expiratoire chez les personnes qui respirent habituellement par la bouche, doivent être considérés, en plus des bioparticules nasales, comme un mode de transmission potentiel de la COVID-19. Les professionnels de la santé buccodentaire craignent, à juste titre, le risque d’exposition dû à la proximité du contact direct et au mode de transmission. L’objectif de ce commentaire est de résumer les recherches menées dans ce domaine et de proposer des stratégies pour limiter la propagation de la COVID-19, notamment dans les cabinets dentaires.

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Brightman, B. K., Q. X. Li, D. J. Trepp, and H. Fan. "Differential disease restriction of Moloney and Friend murine leukemia viruses by the mouse Rmcf gene is governed by the viral long terminal repeat." Journal of Experimental Medicine 174, no. 2 (August 1, 1991): 389–96. http://dx.doi.org/10.1084/jem.174.2.389.

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Neonatal CxD2 (Rmcfr) and Balb/c (Rmcfs) mice inoculated with Moloney murine leukemia virus (M-MuLV) exhibited approximately equivalent time course and pathology for disease. CxD2 mice showed only slightly reduced presence of Moloney mink cell focus-forming virus (M-MCF) provirus as seen by Southern blot analysis compared to Balb/c mice. This lack of restriction for disease and spread of MCF was in sharp contrast to that seen for CxD2 mice inoculated with Friend murine leukemia virus (F-MuLV), where incidence of disease and propagation of MCFs were severely restricted, as previously reported. Inoculation of CxD2 mice with FM-MuLV, a recombinant F-MuLV virus containing M-MuLV LTR sequences (U3 and R), resulted in T cell disease of time course equal to that seen in Balb/c mice; there also was little restriction for propagation of MCFs. This indicated that presence of the M-MuLV long terminal repeat (LTR) was sufficient for propagation of MCFs in CxD2 mice. Differing restriction for F-MuLV vs. M-MuLV in CxD2 mice was explained on the basis of different "MCF propagator cells" for the two viruses. It was suggested that cells propagating F-MCF (e.g., erythroid progenitors) are blocked by endogenous MCF-like gp70env protein, whereas cells propagating M-MCF (e.g., lymphoid) do not express this protein on their surface. F-MuLV disease in CxD2 mice was greatly accelerated when neonates were inoculated with a F-MuLV/F-MCF pseudotypic mixture. However, F-MCF provirus was not detectable or only barely detectable in F-MuLV/F-MCF-induced tumors, suggesting that F-MCF acted indirectly in induction of these tumors.

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Lozovski, V. "Interaction between viral particles and structured metal surface under surface plasmon propagation." Semiconductor Physics Quantum Electronics and Optoelectronics 15, no. 1 (March 29, 2012): 80–82. http://dx.doi.org/10.15407/spqeo15.01.080.

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Ondh-Obame, Jean Alban, Auguste Ndoutoume Ndong, Pamphile Nguema Ndoutoumou, Priscilla Chancia Mindze Assembe, Ignace Davy Mendoume Minko, and Kowir Pambo Bello. "Prévalence du Banana Bunchy Top Disease (BBTD) dans la zone de Ntoum au Gabon." International Journal of Biological and Chemical Sciences 14, no. 3 (June 18, 2020): 739–49. http://dx.doi.org/10.4314/ijbcs.v14i3.8.

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Le Banana Bunchy Top Disease (BBTD) est la maladie virale la plus dévastatrice du bananier impactant considérablement sa production. Le BBTD a été signalé au Gabon pour la première fois par la FAO avec une prévalence de plus de 90%. La présente étude vise à déterminer la prévalence du BBTD, la sévérité et l’importance du vecteur dans la zone de Ntoum. Après une enquête, 1800 pieds de bananiers dans 6 foyers d’infestation, ont été examinés de façon aléatoire avec un système de notation randomisé en transect croisé X. La méthode d’enquête par observation visuelle des symptômes du BBTD avec une échelle de notation de 1 à 5 a été utilisée. Les foyers d’infestation retenus présentent une sévérité de la maladie avancée avec le symptôme visuel de niveau 5 prépondérant et une prévalence moyenne de 21%. Le vecteur, Pentalonia nigronervosa est un insecte présent dans la zone mais à des niveaux d’importance variable. Il serait souhaitable d’évaluer la résistance variétale des Musa spp. et de montrer l’influence des facteurs biotiques et abiotiques sur la propagation de la maladie.Mots clés : Bananier, Pentalonia nigronervosa, foyers d’infestation, sévérité, importance du vecteur. English Title: Prevalence of Banana Bunchy Top Disease (BBTD) in the Ntoum area in Gabon Banana Bunchy Top Disease (BBTD) is the banana's most devastating viral disease, with a significant impact on its production. BBTD was first reported in Gabon by FAO with a prevalence of more than 90%. This study aims to determine the prevalence of BBTD, the severity and importance of the vector in the Ntoum area. After a survey, 1800 feet of banana trees in 6 outbreaks, were examined randomly with a randomized scoring system in transect crossed X. The method of visual observation of BBTD symptoms with a rating scale of 1 to 5 was used. The selected outbreaks have an advanced disease severity with the predominant level 5 visual symptom and an average prevalence of 21%. The vector, Pentalonia nigronervosa is an insect present in the area but at varying levels. It would be desirable to assess the varietal resistance of Musa spp. and to show the influence of biotic and abiotic factors on the spread of the disease.Keywords: Banana, Pentalonia nigronervosa, source of infestation, severity, importance of vector.

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ROSE, Nicolas, and Marie-Frédérique LE POTIER. "L’épizootie de Peste Porcine Africaine : virologie, épidémiologie et perspectives de contrôle." INRAE Productions Animales 33, no. 2 (September 15, 2020): 65–80. http://dx.doi.org/10.20870/productions-animales.2020.33.2.3857.

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La Peste Porcine Africaine (PPA) est une maladie infectieuse émergente des suidés domestiques et sauvages. Cette maladie contagieuse entre suidés, non transmissible à l’Homme, est à l’origine d’un syndrome hémorragique souvent fatal chez les porcs domestiques et les sangliers. L'épizootie qui sévit actuellement en Europe et en Asie a débuté en Géorgie en 2007. La souche virale impliquée, très virulente, appartenant au génotype II, est très résistante dans les viandes et l’environnement. Toutes les souches isolées en Europe comme en Asie dérivent d’une même introduction, même si le virus a évolué vers des formes moins virulentes dans certaines populations de sangliers très localisées. Depuis la Géorgie, le virus s'est propagé dans tout le Caucase et la Fédération de Russie, puis en Ukraine et en Biélorussie en 2013. En janvier 2014, la PPA a atteint les frontières orientales de l'Union européenne et s’est propagée dans les trois États baltes et en Pologne très largement dans les populations de sangliers sauvages, alors que les foyers sporadiques chez les porcs domestiques ont été efficacement contrôlés. Les derniers pays touchés en Europe sont la République Tchèque, la Hongrie, la Moldavie, la Roumanie, la Bulgarie et dernièrement la Belgique (13/09/2018), la Serbie, la Slovaquie et la Grèce en 2020. En Chine, suite au premier cas déclaré le 3/08/18, le virus introduit vraisemblablement à partir de la Russie, donne lieu à une épizootie majeure principalement dans le réservoir domestique, totalement hors de contrôle, et qui s’est propagée aujourd’hui en Mongolie, et plusieurs pays d’Asie du Sud-Est, ainsi que récemment en Inde. L’Homme joue un rôle central en tant que facteur de propagation de par ses activités favorisant ainsi une progression par sauts, parfois sur de très longues distances. Aucun vaccin ou traitement n’est actuellement disponible, la seule méthode de lutte restant la prophylaxie sanitaire et la prévention de l’introduction dans des territoires indemnes comme la France.

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Perissi, Ilaria, Sara Falsini, and Ugo Bardi. "Mechanisms of meme propagation in the mediasphere: a system dynamics model." Kybernetes 48, no. 1 (January 14, 2019): 79–90. http://dx.doi.org/10.1108/k-05-2017-0192.

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Purpose In the age of internet memes spread around the world in very short time, it has been already proved that, in several cases, the mechanism of propagation is very similar to a flu infection. However, this model turns out to be invalid if the spreading is generated by the mass media (TV, radio and the like). This paper aims to explore for the first time this non-viral dynamic (“fallout model”). Design/methodology/approach Two different dynamic models were developed to explain the viral and the mass media-powered meme propagations, and both were tested using data from Google Trends. Findings Viral propagation is not the only mechanism of meme diffusion. Memes can also diffuse by a “fallout” model, in which the susceptible populations are affected by the meme messages almost simultaneously, as it happens in the physical world for a radioactive fallout or for other poisoning agents. Originality/value This study provides a method to determine whether a certain meme has been diffusing by means of its own viral power or has been “planted” as the result of a commercial advertising campaign or a government propaganda operation.

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Muhayimana, Alice, Donatilla Mukamana, Jean Pierre Ndayisenga, Olive Tengera, Josephine Murekezi, Josette Uwacu, Eugenie Mbabazi, and Joyce Musabe. "Implications of COVID-19 Lockdown on Child Preparedness among Rwandan Families." Research Journal of Health Sciences 8, no. 3 (October 9, 2020): 214–20. http://dx.doi.org/10.4314/rejhs.v8i3.8.

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The world is currently facing the fatal viral pandemic called coronavirus disease 2019 (COVID-19), earlier named 2019-novel coronavirus (2019- nCoV). Every country of the world keeps responding to the challenges posed by covid-19 in all aspects of human endeavour with high demand and burden on health care. The report of the first case in Rwanda on 14th March 2020 was accompanied by actions to drive control measures by the government of Rwanda importantly to prevent the spread of COVID-19. Those measures included education on personal preventive behaviours, social distancing and restricting the movement of people locally, nationally and internationally resulting to lockdown that allowed only essential services. Lockdown has particularly affected Rwandan families with pregnant mothers in the context of childbirth preparation in different aspects. This review paper articulates the possible various dimensions of influence of the COVID-19 lockdown on birth preparedness by families and the possible maternal and neonatal health adverse outcomes that may be associated. This is with the intention of helping health care providers and other stakeholders anticipate, track and prepare for appropriate mitigation to reduce maternal-neonatal morbidity and mortality. French title: Implications du verrouillage de COVID-19 sur la préparation des enfants dans les familles RwandaisesLe monde est actuellement confronté à la pandémie virale mortelle appelée maladie à coronavirus 2019 (COVID-19), précédemment appelée 2019-nouveau coronavirus (2019-nCoV). Chaque pays du monde continue de répondre aux défis posés par le Covid-19 dans tous les aspects de l'activité humaine avec une forte demande et un fardeau sur les soins de santé. Le rapport du premier cas au Rwanda le 14e mars 2020 a été accompagné d'actions à conduire des mesures de contrôle par le gouvernement du Rwanda important pour prévenir la propagation de Covid-19. Ces mesures comprenaient une éducation sur les comportements personnels de prévention, la distanciation sociale et la restriction de la circulation des personnes aux niveaux local, national et international, entraînant un verrouillage qui n'autorisait que les services essentiels. Le verrouillage a particulièrement affecté les familles Rwandaises de mères enceintes dans le cadre de la préparation à l'accouchement sous différents aspects. Cet article de synthèse articule les différentes dimensions possibles de l'influence du verrouillage du COVID-19 sur la préparation à la naissance des familles et les éventuels effets indésirables sur la santé maternelle et néonatale qui peuvent être associés. Ceci dans le but d'aider les prestataires de soins de santé et les autres parties prenantes à anticiper, suivre et préparer des mesures d'atténuation appropriées pour réduire la morbidité et la mortalité materné-néonatales.

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Takamatsu, Yuki, Kouichi Morita, and Daisuke Hayasaka. "A Single Amino Acid Substitution in the NS2A Protein of Japanese Encephalitis Virus Affects Virus PropagationIn Vitrobut NotIn Vivo." Journal of Virology 89, no. 11 (March 18, 2015): 6126–30. http://dx.doi.org/10.1128/jvi.00370-15.

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We identified a unique amino acid of NS2A113, phenylalanine, that affects the efficient propagation of two Japanese encephalitis virus strains, JaTH160 and JaOArS982, in neuroblastoma Neuro-2a cells but not in cell lines of extraneural origin. This amino acid did not affect viral loads in the brain or survival curves in mice. These findings suggest that virus propagationin vitromay not reflect the level of virus neuroinvasivenessin vivo.

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Hanson, Lars A., Ivar Lonnroth, Stefan Lange, Jan Bjersing, and U. I. Dahlgren. "Nutrition Resistance to Viral Propagation." Nutrition Reviews 58 (April 27, 2009): S31—S37. http://dx.doi.org/10.1111/j.1753-4887.2000.tb07801.x.

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Kudryashova, Olga B., Evgeny V. Muravlev, Aleksandra A. Antonnikova, and Sergey S. Titov. "Propagation of viral bioaerosols indoors." PLOS ONE 16, no. 1 (January 5, 2021): e0244983. http://dx.doi.org/10.1371/journal.pone.0244983.

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Here we look into the spread of aerosols indoors that may potentially carry viruses. Many viruses, including the novel SARS-CoV-2, are known to spread via airborne and air-dust pathways. From the literature data and our research on the propagation of fine aerosols, we simulate herein the carryover of viral aerosols in indoor air. We demonstrate that a lot of fine droplets released from an infected person’s coughing, sneezing, or talking propagate very fast and for large distances indoors, as well as bend around obstacles, lift up and down over staircases, and so on. This study suggests equations to evaluate the concentration of those droplets, depending on time and distance from the source of infection. Estimates are given for the safe distance to the source of infection, and available methods for neutralizing viral aerosols indoors are considered.

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Yin, John. "A quantifiable phenotype of viral propagation." Biochemical and Biophysical Research Communications 174, no. 2 (January 1991): 1009–14. http://dx.doi.org/10.1016/0006-291x(91)91519-i.

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Budzanivska, I. G., and F. Demyanenko. "Inhibition of Solanaceae plants by combined effect of increased concentrations of heavy metals and viral infection." Plant Protection Science 38, SI 2 - 6th Conf EFPP 2002 (December 31, 2017): 452–54. http://dx.doi.org/10.17221/10521-pps.

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On plants of a Solanaceae family cultivated on a ground with increased concentrations of metals (Cu = 10; Pb = 21.5; Zn = 13.2 mg/kg) was shown both propagation and development depressing and decreasing of common protein. The superposition of a virus infection (TMV, PVX) results in considerable accumulation of viruses and early plants death. The contamination of soil by heavy metals results in plants propagation and development depressing, that in turn entails considerable development of viral and other infections resulting in crop losses.

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Li, Guohui, Xinyu Qi, Zhaoyang Hu, and Qi Tang. "Mechanisms Mediating Nuclear Trafficking Involved in Viral Propagation by DNA Viruses." Viruses 11, no. 11 (November 7, 2019): 1035. http://dx.doi.org/10.3390/v11111035.

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Typical viral propagation involves sequential viral entry, uncoating, replication, gene transcription and protein synthesis, and virion assembly and release. Some viral proteins must be transported into host nucleus to facilitate viral propagation, which is essential for the production of mature virions. During the transport process, nuclear localization signals (NLSs) play an important role in guiding target proteins into nucleus through the nuclear pore. To date, some classical nuclear localization signals (cNLSs) and non-classical NLSs (ncNLSs) have been identified in a number of viral proteins. These proteins are involved in viral replication, expression regulation of viral genes and virion assembly. Moreover, other proteins are transported into nucleus with unknown mechanisms. This review highlights our current knowledge about the nuclear trafficking of cellular proteins associated with viral propagation.

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Li, Li, Hui Xia, and Ye Li. "A Unique Perspective on Viral Propagation--Social Attributes." Procedia Computer Science 174 (2020): 256–62. http://dx.doi.org/10.1016/j.procs.2020.06.082.

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Giorda, Kristina M., and Daniel N. Hebert. "Viroporins Customize Host Cells for Efficient Viral Propagation." DNA and Cell Biology 32, no. 10 (October 2013): 557–64. http://dx.doi.org/10.1089/dna.2013.2159.

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Morgan, Wayne. "Viral Respiratory Infection in Infancy: Provocation or Propagation?" Seminars in Respiratory and Critical Care Medicine 11, no. 04 (October 1990): 306–13. http://dx.doi.org/10.1055/s-2007-1006214.

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Florez, Paola M., October M. Sessions, Eric J. Wagner, Matthias Gromeier, and Mariano A. Garcia-Blanco. "The Polypyrimidine Tract Binding Protein Is Required for Efficient Picornavirus Gene Expression and Propagation." Journal of Virology 79, no. 10 (May 15, 2005): 6172–79. http://dx.doi.org/10.1128/jvi.79.10.6172-6179.2005.

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ABSTRACT Mammalian host factors required for efficient viral gene expression and propagation have been often recalcitrant to genetic analysis. A case in point is the function of cellular factors that trans-activate internal ribosomal entry site (IRES)-driven translation, which is operative in many positive-stranded RNA viruses, including all picornaviruses. These IRES trans-acting factors have been elegantly studied in vitro, but their in vivo importance for viral gene expression and propagation has not been widely confirmed experimentally. Here we use RNA interference to deplete mammalian cells of one such factor, the polypyrimidine tract binding protein, and test its requirement in picornavirus gene expression and propagation. Depletion of the polypyrimidine tract binding protein resulted in a marked delay of particle propagation and significantly decreased synthesis and accumulation of viral proteins of poliovirus and encephalomyocarditis virus. These effects could be partially restored by expression of an RNA interference-resistant exogenous polypyrimidine tract binding protein. These data indicate a critical role for the polypyrimidine tract binding protein in picornavirus gene expression and strongly suggest a requirement for efficient IRES-dependent translation.

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Campbell, Stephanie A., Matthew Mulvey, Ian Mohr, and Matthias Gromeier. "Attenuation of Herpes Simplex Virus Neurovirulence with Picornavirus cis-Acting Genetic Elements." Journal of Virology 81, no. 2 (November 1, 2006): 791–99. http://dx.doi.org/10.1128/jvi.00714-06.

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ABSTRACT Viral pathogenesis depends on a suitable milieu in target host cells permitting viral gene expression, propagation, and spread. In many instances, viral genomes can be manipulated to select for propagation in certain tissues or cell types. This has been achieved for the neurotropic poliovirus (PV) by exchange of the internal ribosomal entry site (IRES), which is responsible for translation of the uncapped plus-strand RNA genome. The IRES of human rhinovirus type 2 (HRV2) confers neuron-specific replication deficits to PV but has no effect on viral propagation in malignant glioma cells. We report here that placing the critical γ1 34.5 virulence genes of herpes simplex virus type 1 (HSV) under translation control of the HRV2 IRES results in neuroattenuation in mice. In contrast, IRES insertion permits HSV propagation in malignant glioma cell lines that do not support replication of HSV recombinants carrying γ1 34.5 deletions. Our observations indicate that the conditions for alternative translation initiation at the HRV2 IRES in malignant glioma cells differ from those in normal central nervous system (CNS) cells. Picornavirus regulatory sequences mediating cell type-specific gene expression in the CNS can be utilized to target cancerous cells at the level of translation regulation outside their natural context.

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Freeman, Mark, James McVittie, Iryna Sivak, and Jianhong Wu. "Viral information propagation in the Digg online social network." Physica A: Statistical Mechanics and its Applications 415 (December 2014): 87–94. http://dx.doi.org/10.1016/j.physa.2014.06.011.

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Löhner, Rainald, Harbir Antil, Sergio Idelsohn, and Eugenio Oñate. "Detailed simulation of viral propagation in the built environment." Computational Mechanics 66, no. 5 (August 5, 2020): 1093–107. http://dx.doi.org/10.1007/s00466-020-01881-7.

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SHEARER, ADRIENNE E. H., DALLAS G. HOOVER, and KALMIA E. KNIEL. "Effect of Bacterial Cell-Free Supernatants on Infectivity of Norovirus Surrogates." Journal of Food Protection 77, no. 1 (January 1, 2014): 145–49. http://dx.doi.org/10.4315/0362-028x.jfp-13-204.

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Bacterial metabolic products were evaluated for inhibitory effects on viral propagation in cell culture. Cell-free supernatants (CFS) were prepared from growth of Enterococcus faecalis ATCC 19433, Pseudomonas fluorescens ATCC 13525, Escherichia coli 08, Staphylococcus epidermidis ATCC 12228, Bacillus subtilis 168, Bacillus coagulans 185A, B. coagulans 7050, Clostridium sporogenes PA3679, and a commercial probiotic mixture of Lactobacillus acidophilus, Lactobacillus rhamnosus, Bifidobacterium bifidum, Lactobacillus salivarius, and Streptococcus thermophilus in microbiological medium or milk. The inhibitory effects of CFS on the propagation of murine norovirus 1 and Tulane virus in RAW 264.7 and LLCMK2 cells, respectively, were evaluated in the continuous presence of CFS or after exposure of host cells to CFS. Slight inhibition of viral propagation was observed for murine norovirus and Tulane virus in the continuous presence of CFS of B. subtilis 168 and E. faecalis 19433, respectively. CFS cytotoxicity was also determined by microscopic examination. Virus persisted in the CFS that demonstrated cytotoxic effects, suggesting a lack of direct effect of CFS on virions. The viral propagation indicates a general lack of competitive inhibition by bacterial extracellular products and bears significance in understanding the persistence of virus in food and human systems shared by bacteria that are recognized for their colonization and competitive capabilities.

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Merrill, Melinda K., Elena Y. Dobrikova, and Matthias Gromeier. "Cell-Type-Specific Repression of Internal Ribosome Entry Site Activity by Double-Stranded RNA-Binding Protein 76." Journal of Virology 80, no. 7 (April 1, 2006): 3147–56. http://dx.doi.org/10.1128/jvi.80.7.3147-3156.2006.

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ABSTRACT Translation of picornavirus plus-strand RNA genomes occurs via internal ribosomal entry at highly structured 5′ untranslated regions. In addition to canonical translation factors, translation rate is likely influenced by supplementary host and viral trans-acting factors. We previously reported that insertion of a heterologous human rhinovirus type 2 internal ribosomal entry site (IRES) into the poliovirus (PV) genome, generating the chimeric virus PV-RIPO, selectively abrogates viral translation and propagation in neurons, which eliminate poliovirus's signature neuropathogenicity. While severely deficient in cells of neuronal lineage, the rhinovirus IRES promotes efficient propagation of PV-RIPO in cancer cells. Tumor-specific IRES function can be therapeutically exploited to direct viral cytotoxicity to cancer cells. Neuron-glioma heterokaryon analysis implicates neuronal trans-dominant inhibition in this effect, suggesting that host trans-acting factors repress IRES function in a cell-type-specific manner. We identified a set of proteins from neuronal cells with affinity for the rhinovirus IRES, including double-stranded RNA-binding protein 76 (DRBP76). DRBP76 associates with the IRES in neuronal but not in malignant glioma cells. Moreover, DRBP76 depletion in neuronal cells enhances rhinovirus IRES-driven translation and virus propagation. Our observations suggest that cell-type-specific association of DRBP76 with the rhinovirus IRES represses PV-RIPO translation and propagation in neuronal cells.

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Teale, Alastair, Stephanie Campbell, Nick Van Buuren, Wendy C. Magee, Kelly Watmough, Brianne Couturier, Robyn Shipclark, and Michele Barry. "Orthopoxviruses Require a Functional Ubiquitin-Proteasome System for Productive Replication." Journal of Virology 83, no. 5 (December 24, 2008): 2099–108. http://dx.doi.org/10.1128/jvi.01753-08.

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ABSTRACT Cellular homeostasis depends on an intricate balance of protein expression and degradation. The ubiquitin-proteasome pathway plays a crucial role in specifically targeting proteins tagged with ubiquitin for destruction. This degradation can be effectively blocked by both chemically synthesized and natural proteasome inhibitors. Poxviruses encode a number of proteins that exploit the ubiquitin-proteasome system, including virally encoded ubiquitin molecules and ubiquitin ligases, as well as BTB/kelch proteins and F-box proteins, which interact with cellular ubiquitin ligases. Here we show that poxvirus infection was dramatically affected by a range of proteasome inhibitors, including MG132, MG115, lactacystin, and bortezomib (Velcade). Confocal microscopy demonstrated that infected cells treated with MG132 or bortezomib lacked viral replication factories within the cytoplasm. This was accompanied by the absence of late gene expression and DNA replication; however, early gene expression occurred unabated. Proteasomal inhibition with MG132 or bortezomib also had dramatic effects on viral titers, severely blocking viral replication and propagation. The effects of MG132 on poxvirus infection were reversible upon washout, resulting in the production of late genes and viral replication factories. Significantly, the addition of an ubiquitin-activating enzyme (E1) inhibitor had a similar affect on late and early protein expression. Together, our data suggests that a functional ubiquitin-proteasome system is required during poxvirus infection.

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Bandilovska, Ivona, Simon P. Keam, Cristina Gamell, Claudia Machicado, Sue Haupt, and Ygal Haupt. "E6AP goes viral: the role of E6AP in viral- and non-viral-related cancers." Carcinogenesis 40, no. 6 (April 10, 2019): 707–14. http://dx.doi.org/10.1093/carcin/bgz072.

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Abstract Since its discovery, the E3 ubiquitin ligase E6-associated protein (E6AP) has been studied extensively in two pathological contexts: infection by the human papillomavirus (HPV), and the neurodevelopmental disorder, Angelman syndrome. Vital biological links between E6AP and other viruses, namely hepatitis C virus and encephalomyocarditis virus, have been recently uncovered. Critically, oncogenic E6AP activities have been demonstrated to contribute to cancers of both viral and non-viral origins. HPV-associated cancers serve as the primary example of E6AP involvement in cancers driven by viruses. Studies over the past few years have exposed a role for E6AP in non-viral-related cancers. This has been demonstrated in B-cell lymphoma and prostate cancers, where oncogenic E6AP functions drive these cancers by acting on key tumour suppressors. In this review we discuss the role of E6AP in viral infection, viral propagation and viral-related cancer. We discuss processes affected by oncogenic E6AP, which promote cancers of viral and non-viral aetiology. Overall, recent findings support the role of oncogenic E6AP in disrupting key cellular processes, including tumour suppression and the immune response. E6AP is consequently emerging as an attractive therapeutic target for a number of specific cancers.

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Tang, Qi, Peng Wu, Huiqing Chen, and Guohui Li. "Pleiotropic roles of the ubiquitin-proteasome system during viral propagation." Life Sciences 207 (August 2018): 350–54. http://dx.doi.org/10.1016/j.lfs.2018.06.014.

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Capitán, José A., José A. Cuesta, Susanna C. Manrubia, and Jacobo Aguirre. "Severe Hindrance of Viral Infection Propagation in Spatially Extended Hosts." PLoS ONE 6, no. 8 (August 23, 2011): e23358. http://dx.doi.org/10.1371/journal.pone.0023358.

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Coscia, Michele. "Popularity spikes hurt future chances for viral propagation of protomemes." Communications of the ACM 61, no. 1 (December 27, 2017): 70–77. http://dx.doi.org/10.1145/3158227.

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Dáder, Beatriz, Christiane Then, Edwige Berthelot, Marie Ducousso, James C. K. Ng, and Martin Drucker. "Insect transmission of plant viruses: Multilayered interactions optimize viral propagation." Insect Science 24, no. 6 (July 18, 2017): 929–46. http://dx.doi.org/10.1111/1744-7917.12470.

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Thavachelvam, Karthiga, Hans Henrik Gad, Mikkel Søes Ibsen, Philippe Desprès, Marianne Hokland, Rune Hartmann, and Helle Kristiansen. "Rapid Uptake and Inhibition of Viral Propagation by Extracellular OAS1." Journal of Interferon & Cytokine Research 35, no. 5 (May 2015): 359–66. http://dx.doi.org/10.1089/jir.2014.0140.

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Wang, Lin, and Brendan C. Wood. "An epidemiological approach to model the viral propagation of memes." Applied Mathematical Modelling 35, no. 11 (November 2011): 5442–47. http://dx.doi.org/10.1016/j.apm.2011.04.035.

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Zhang, Chunming. "Global Behavior of a Computer Virus Propagation Model on Multilayer Networks." Security and Communication Networks 2018 (2018): 1–9. http://dx.doi.org/10.1155/2018/2153195.

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This paper presents a new linear computer viruses propagation model on multilayer networks to explore the mechanism of computer virus propagation. Theoretical analysis demonstrates that the maximum eigenvalue of the sum of all the subnetworks is a vital factor in determining the viral prevalence. And then, a new sufficient condition for the global stability of virus-free equilibrium has been obtained. The persistence of computer virus propagation system has also been proved. Eventually, some numerical simulation results verify the main conclusions of the theoretical analysis.

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Tran, Giao V. Q., Trang T. D. Luong, Eun-Mee Park, Jong-Wook Kim, Jae-Woong Choi, Chorong Park, Yun-Sook Lim, and Soon B. Hwang. "Nonstructural 5A Protein of Hepatitis C Virus Regulates Soluble Resistance-Related Calcium-Binding Protein Activity for Viral Propagation." Journal of Virology 90, no. 6 (December 30, 2015): 2794–805. http://dx.doi.org/10.1128/jvi.02493-15.

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ABSTRACTHepatitis C virus (HCV) is a major cause of chronic liver disease and is highly dependent on cellular proteins for virus propagation. To identify the cellular factors involved in HCV propagation, we recently performed protein microarray assays using the HCV nonstructural 5A (NS5A) protein as a probe. Of 90 cellular protein candidates, we selected the soluble resistance-related calcium-binding protein (sorcin) for further characterization. Sorcin is a calcium-binding protein and is highly expressed in certain cancer cells. We verified that NS5A interacted with sorcin through domain I of NS5A, and phosphorylation of the threonine residue 155 of sorcin played a crucial role in protein interaction. Small interfering RNA (siRNA)-mediated knockdown of sorcin impaired HCV propagation. Silencing of sorcin expression resulted in a decrease of HCV assembly without affecting HCV RNA and protein levels. We further demonstrated that polo-like kinase 1 (PLK1)-mediated phosphorylation of sorcin was increased by NS5A. We showed that both phosphorylation and calcium-binding activity of sorcin were required for HCV propagation. These data indicate that HCV modulates sorcin activity via NS5A protein for its own propagation.IMPORTANCESorcin is a calcium-binding protein and regulates intracellular calcium homeostasis. HCV NS5A interacts with sorcin, and phosphorylation of sorcin is required for protein interaction. Gene silencing of sorcin impaired HCV propagation at the assembly step of the HCV life cycle. Sorcin is phosphorylated by PLK1 via protein interaction. We showed that sorcin interacted with both NS5A and PLK1, and PLK1-mediated phosphorylation of sorcin was increased by NS5A. Moreover, calcium-binding activity of sorcin played a crucial role in HCV propagation. These data provide evidence that HCV regulates host calcium metabolism for virus propagation, and thus manipulation of sorcin activity may represent a novel therapeutic target for HCV.

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Dangsagul, Worawat, Kriengsak Ruchusatsawat, Apiwat Tawatsin, Don Changsom, Pirom Noisumdaeng, Sukontip Putchakarn, Chayawat Phatihattakorn, Prasert Auewarakul, and Pilaipan Puthavathana. "Zika virus isolation, propagation, and quantification using multiple methods." PLOS ONE 16, no. 7 (July 30, 2021): e0255314. http://dx.doi.org/10.1371/journal.pone.0255314.

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Zika virus (ZIKV) was isolated from the archival urine, serum, and autopsy specimens by intrathoracic inoculation of Toxorhynchitis splendens and followed by three blind sub-passaging in C6/36 mosquito cells. The virus isolates were identified using an immunofluorescence assay and real-time reverse transcription-polymerase chain reaction (real-time RT-PCR). This study analyzed 11 ZIKV isolates. One isolate (0.6%) was obtained from 171 urine samples, eight (8.7%) from 92 serum samples and two from tissues of an abortive fetus. After propagation in C6/36 cells, ZIKV was titrated by plaque and focus forming unit (FFU) assays in Vero cell monolayers, and viral genomes were determined via real-time and digital RT-PCR. Plaque and FFU assay quantitations were comparable, with the amount of infectious viruses averaging 106−107 PFU or FFU/ml. Real-time RT-PCR semi-quantified the viral genome numbers, with Ct values varying from 12 to 14. Digital RT-PCR, which precisely determines the numbers of the viral genomes, consistently averaged 10–100 times higher than the number of infectious units. There was good correlation between the results of these titration methods. Therefore, the selection of a method should be based on the objectives of each research studies.

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Nasser, Roudaina, Mireia Pelegrin, Henri-Alexandre Michaud, Marc Plays, Marc Piechaczyk, and Laurent Gros. "Long-Lasting Protective Antiviral Immunity Induced by Passive Immunotherapies Requires both Neutralizing and Effector Functions of the Administered Monoclonal Antibody." Journal of Virology 84, no. 19 (July 7, 2010): 10169–81. http://dx.doi.org/10.1128/jvi.00568-10.

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ABSTRACT Using FrCasE retrovirus-infected newborn mice as a model system, we have shown recently that a long-lasting antiviral immune response essential for healthy survival emerges after a short treatment with a neutralizing (667) IgG2a isotype monoclonal antibody (MAb). This suggested that the mobilization of adaptive immunity by administered MAbs is key for the success in the long term for the MAb-based passive immunotherapy of chronic viral infections. We have addressed here whether the anti-FrCasE protective endogenous immunity is the mere consequence of viral propagation blunting, which would simply give time to the immune system to react, and/or to actual immunomodulation by the MAb during the treatment. To this aim, we have compared viral replication, disease progression, and antiviral immune responses between different groups of infected mice: (i) mice treated with either the 667 MAb, its F(ab′)2 fragment, or an IgM (672) with epitopic specificity similar to that of 667 but displaying different effector functions, and (ii) mice receiving no treatment but infected with a low viral inoculum reproducing the initial viral expansion observed in their infected/667 MAb-treated counterparts. Our data show that the reduction of FrCasE propagation is insufficient on its own to induce protective immunity and support a direct immunomodulatory action of the 667 MAb. Interestingly, they also point to sequential actions of the administered MAb. In a first step, viral propagation is exclusively controlled by 667 neutralizing activity, and in a second one, this action is complemented by FcγR-binding-dependent mechanisms, which most likely combine infected cell cytolysis and the modulation of the antiviral endogenous immune response. Such complementary effects of administered MAbs must be taken into consideration for the improvement of future antiviral MAb-based immunotherapies.

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Mori, Yoshio, Tamaki Okabayashi, Tetsuo Yamashita, Zijiang Zhao, Takaji Wakita, Kotaro Yasui, Futoshi Hasebe, et al. "Nuclear Localization of Japanese Encephalitis Virus Core Protein Enhances Viral Replication." Journal of Virology 79, no. 6 (March 15, 2005): 3448–58. http://dx.doi.org/10.1128/jvi.79.6.3448-3458.2005.

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ABSTRACT Japanese encephalitis virus (JEV) core protein was detected in both the nucleoli and cytoplasm of mammalian and insect cell lines infected with JEV or transfected with the expression plasmid of the core protein. Mutation analysis revealed that Gly42 and Pro43 in the core protein are essential for the nuclear and nucleolar localization. A mutant M4243 virus in which both Gly42 and Pro43 were replaced by Ala was recovered by plasmid-based reverse genetics. In C6/36 mosquito cells, the M4243 virus exhibited RNA replication and protein synthesis comparable to wild-type JEV, whereas propagation in Vero cells was impaired. The mutant core protein was detected in the cytoplasm but not in the nucleus of either C6/36 or Vero cell lines infected with the M4243 virus. The impaired propagation of M4243 in mammalian cells was recovered by the expression of wild-type core protein in trans but not by that of the mutant core protein. Although M4243 mutant virus exhibited a high level of neurovirulence comparable to wild-type JEV in spite of the approximately 100-fold-lower viral propagation after intracerebral inoculation to 3-week-old mice of strain Jcl:ICR, no virus was recovered from the brain after intraperitoneal inoculation of the mutant. These results indicate that nuclear localization of JEV core protein plays crucial roles not only in the replication in mammalian cells in vitro but also in the pathogenesis of encephalitis induced by JEV in vivo.

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Kajon, Adriana E., Xiaoxin Li, Gabriel Gonzalez, Susan Core, Helga Hofmann-Sieber, and Shuguang Leng. "Isolation and initial propagation of guinea pig adenovirus (GPAdV) in Cavia porcellus cell lines." F1000Research 8 (September 5, 2019): 1597. http://dx.doi.org/10.12688/f1000research.20135.1.

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Background: The lack of adequate in vitro systems to isolate and propagate guinea pig adenovirus (GPAdV), a prevalent cause of respiratory illness of varaible severity in laboratory guinea pig colonies worldwide, has precluded its formal characterization to allow for the development of comprehensive diagnostic assays, and for the execution of complex pathogenesis and basic virology studies. Methods: Two strains of GPAdV were isolated in guinea pig (Cavia porcellus) cell cultures from frozen archival infected animal tissue originated from colony outbreaks of pneumonia in Australia and the Czech Republic in 1996. Results: Commercially available guinea pig cell lines from colorectal carcinoma (GPC-16), fetal fibroblast (104-C1) and lung fibroblast (JH4 C1), and the tracheal epithelial cell line GPTEC-T developed in this study were able to support viral infection and early propagation. Sufficient viral DNA was recovered from cell cultures to PCR-amplify and obtain sequence data for the complete hexon gene and partial DNA polymerase and penton base genes. Phylogenetic analysis for the three regions of the genome provided strong evidence confirming GPAdV as a unique species in the genus Mastadenovirus. Conclusions: This study demonstrated the feasibility of propagating GPAdV in cultures of immortalized lines of GP cells of a variety of types, thus establishing a critical foundation for the development of a robust culture platform for virus stock production and titration. The generation and analysis of whole GPAdV genome sequences will provide additional data for a comprehensive description of the genetic organization of the viral genome and for a better assessment of genetic diversity between the two isolated strains.

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Kajon, Adriana E., Xiaoxin Li, Gabriel Gonzalez, Susan Core, Helga Hofmann-Sieber, and Shuguang Leng. "Isolation and initial propagation of guinea pig adenovirus (GPAdV) in Cavia porcellus cell lines." F1000Research 8 (March 16, 2020): 1597. http://dx.doi.org/10.12688/f1000research.20135.2.

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Background: The lack of adequate in vitro systems to isolate and propagate guinea pig adenovirus (GPAdV), a prevalent cause of respiratory illness of varaible severity in laboratory guinea pig colonies worldwide, has precluded its formal characterization to allow for the development of comprehensive diagnostic assays, and for the execution of complex pathogenesis and basic virology studies. Methods: Two strains of GPAdV were isolated in guinea pig (Cavia porcellus) cell cultures from frozen archival infected animal tissue originated from colony outbreaks of pneumonia in Australia and the Czech Republic in 1996. Results: Commercially available guinea pig cell lines from colorectal carcinoma (GPC-16), fetal fibroblast (104-C1) and lung fibroblast (JH4 C1), and the tracheal epithelial cell line GPTEC-T developed in this study were able to support viral infection and early propagation. Sufficient viral DNA was recovered from cell cultures to PCR-amplify and obtain sequence data for the complete hexon gene and partial DNA polymerase and penton base genes. Phylogenetic analysis for the three regions of the genome provided strong evidence confirming GPAdV as a unique species in the genus Mastadenovirus. Conclusions: This study demonstrated the feasibility of propagating GPAdV in cultures of immortalized lines of GP cells of a variety of types, thus establishing a critical foundation for the development of a robust culture platform for virus stock production and titration. The generation and analysis of whole GPAdV genome sequences will provide additional data for a comprehensive description of the genetic organization of the viral genome and for a better assessment of genetic diversity between the two isolated strains.

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Strazic Geljic, Ivana, Paola Kucan Brlic, Lucija Musak, Dubravka Karner, Andreja Ambriović-Ristov, Stipan Jonjic, Peter Schu, and Tihana Lenac Rovis. "Viral Interactions with Adaptor-Protein Complexes: A Ubiquitous Trait among Viral Species." International Journal of Molecular Sciences 22, no. 10 (May 17, 2021): 5274. http://dx.doi.org/10.3390/ijms22105274.

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Numerous viruses hijack cellular protein trafficking pathways to mediate cell entry or to rearrange membrane structures thereby promoting viral replication and antagonizing the immune response. Adaptor protein complexes (AP), which mediate protein sorting in endocytic and secretory transport pathways, are one of the conserved viral targets with many viruses possessing AP-interacting motifs. We present here different mechanisms of viral interference with AP complexes and the functional consequences that allow for efficient viral propagation and evasion of host immune defense. The ubiquity of this phenomenon is evidenced by the fact that there are representatives for AP interference in all major viral families, covered in this review. The best described examples are interactions of human immunodeficiency virus and human herpesviruses with AP complexes. Several other viruses, like Ebola, Nipah, and SARS-CoV-2, are pointed out as high priority disease-causative agents supporting the need for deeper understanding of virus-AP interplay which can be exploited in the design of novel antiviral therapies.

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Vincent, Theresa, Ben-Gary Harvey, Suzanne M. Hogan, Christopher J. Bailey, Ronald G. Crystal, and Philip L. Leopold. "Rapid Assessment of Adenovirus Serum Neutralizing Antibody Titer Based on Quantitative, Morphometric Evaluation of Capsid Binding and Intracellular Trafficking: Population Analysis of Adenovirus Capsid Association with Cells Is Predictive of Adenovirus Infectivity." Journal of Virology 75, no. 3 (February 1, 2001): 1516–21. http://dx.doi.org/10.1128/jvi.75.3.1516-1521.2001.

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ABSTRACT Neutralizing antiviral antibodies are typically detected on the basis of inhibition of viral function, such as propagation of a viral infection or inhibition of viral gene expression. Evidence is presented that anti-adenovirus neutralizing antibodies can be evaluated by analysis of cell-associated capsids or by analysis of intracellular trafficking of the capsids within 1 h after infection. Quantitative analyses of these morphologic parameters represent rapid, broadly applicable, functional assays for the detection of anti-adenovirus neutralizing antibodies.

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NOJIRI, NORIYUKI. "Side effects of blood transfusion. Viral hepatitis propagation by blood transfusion." Japanese journal of extra-corporeal technology 24, no. 1 (1997): 1–8. http://dx.doi.org/10.7130/hokkaidoshakai.24.1.

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Zeitler, Benjamin, and Ingrid Rapp. "Determination of Infectious Bovine Viral Diarrhea Virus in Bovine Lung Lavages by a Combination of Virus Propagation in Cell Culture and Quantitative Real-Time PCR." ISRN Virology 2013 (June 20, 2013): 1–9. http://dx.doi.org/10.5402/2013/751904.

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Material of bovine origin is often used in biotechnological applications. Bovine viral diarrhea virus (BVDV) is one of the major viral contaminants, and not only detection and inactivation but also quantification of the viral load in bovine starting material is required by the regulatory agencies. Here, we investigated combined virus propagation in cell culture and quantitative real-time PCR (qRT-PCR) for the applicability to detect and estimate low BVDV titers in bovine lung lavages, the source material for manufacturing pulmonary surfactant. qRT-PCR analyses of the crude lung lavages were performed and qRT-PCR calibration curves based on infective viral doses (TCID50/mL) were generated with a detection limit of 100 TCID50/mL. Lung lavages were inoculated on susceptible MDBK cells and cell culture samples were again analyzed by qRT-PCR. Immunofluorescence staining was performed to prove qRT-PCR results. Interestingly, initial BVDV contaminations in lung lavages were below qRT-PCR detection limit. An amplification step in cell culture enabled BVDV propagation to levels detectable by qRT-PCR. In comparison with the qRT-PCR calibration curve and control experiments with defined inoculation doses, the estimation of minor BVDV contaminations in lung lavages was possible. Both techniques can be successfully combined to estimate the viral load in dilute sample material.

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Takagi, Hirotaka, Tomoichiro Oka, Takashi Shimoike, Hiroyuki Saito, Takayuki Kobayashi, Tomoko Takahashi, Chika Tatsumi, et al. "Human sapovirus propagation in human cell lines supplemented with bile acids." Proceedings of the National Academy of Sciences 117, no. 50 (November 30, 2020): 32078–85. http://dx.doi.org/10.1073/pnas.2007310117.

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Human sapoviruses (HuSaVs) cause acute gastroenteritis similar to human noroviruses. Although HuSaVs were discovered four decades ago, no HuSaV has been grown in vitro, which has significantly impeded the understanding of viral biology and the development of antiviral strategies. In this study, we identified two susceptible human cell lines, that originated from testis and duodenum, that support HuSaV replication and found that replication requires bile acids. HuSaVs replicated more efficiently in the duodenum cell line, and viral RNA levels increased up to ∼6 log10-fold. We also detected double-stranded RNA, viral nonstructural and structural proteins in the cell cultures, and intact HuSaV particles. We confirmed the infectivity of progeny viruses released into the cell culture supernatants by passaging. These results indicate the successful growth of HuSaVs in vitro. Additionally, we determined the minimum infectious dose and tested the sensitivities of HuSaV GI.1 and GII.3 to heat and ultraviolet treatments. This system is inexpensive, scalable, and reproducible in different laboratories, and can be used to investigate mechanisms of HuSaV replication and to evaluate antivirals and/or disinfection methods for HuSaVs.

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Xiang, Pinhao, Yasir Mohamud, and Honglin Luo. "SNAP47 Interacts with ATG14 to Promote VP1 Conjugation and CVB3 Propagation." Cells 10, no. 8 (August 20, 2021): 2141. http://dx.doi.org/10.3390/cells10082141.

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Coxsackievirus B3 (CVB3), an enterovirus (EV) in the family of Picornaviridae, is a global human pathogen for which effective antiviral treatments and vaccines are lacking. Previous research demonstrated that EV-D68 downregulated the membrane fusion protein SNAP47 (synaptosome associated protein 47) and SNAP47 promoted EV-D68 replication via regulating autophagy. In the current study, we investigated the interplay between CVB3 and cellular SNAP47 using HEK293T/HeLa cell models. We showed that, upon CVB3 infection, protein levels of SNAP47 decreased independent of the activity of virus-encoded proteinase 3C. We further demonstrated that the depletion of SNAP47 inhibited CVB3 infection, indicating a pro-viral function of SNAP47. Moreover, we found that SNAP47 co-localizes with the autophagy-related protein ATG14 on the cellular membrane fractions together with viral capsid protein VP1, and expression of SNAP47 or ATG14 enhanced VP1 conjugation. Finally, we revealed that disulfide interactions had an important role in strengthening VP1 conjugation. Collectively, our study elucidated a mechanism by which SNAP47 and ATG14 promoted CVB3 propagation through facilitating viral capsid assembly.

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Piccone, Maria E., Yanan Feng, Annie C. Y. Chang, Ronen Mosseri, Quan Lu, Gerald F. Kutish, Zhiqiang Lu, et al. "Identification of Cellular Genes Affecting the Infectivity of Foot-and-Mouth Disease Virus." Journal of Virology 83, no. 13 (April 15, 2009): 6681–88. http://dx.doi.org/10.1128/jvi.01729-08.

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ABSTRACT Foot-and-mouth disease virus (FMDV) produces one of the most infectious of all livestock diseases, causing extensive economic loss in areas of breakout. Like other viral pathogens, FMDV recruits proteins encoded by host cell genes to accomplish the entry, replication, and release of infectious viral particles. To identify such host-encoded proteins, we employed an antisense RNA strategy and a lentivirus-based library containing approximately 40,000 human expressed sequence tags (ESTs) to randomly inactivate chromosomal genes in a bovine kidney cell line (LF-BK) that is highly susceptible to FMDV infection and then isolated clones that survived multiple rounds of exposure to the virus. Here, we report the identification of ESTs whose expression in antisense orientation limited host cell killing by FMDV and restricted viral propagation. The role of one such EST, that of ectonucleoside triphosphate diphosphohydrolase 6 (NTPDase6; also known as CD39L2), a membrane-associated ectonucleoside triphosphate diphosphohydrolase that previously was not suspected of involvement in the propagation of viral pathogens and which we now show is required for normal synthesis of FMDV RNA and proteins, is described in this report.

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Zhao, Tian-Fang, Wei-Neng Chen, Xin-Xin Ma, and Xiao-Kun Wu. "Evolutionary Computation in Social Propagation over Complex Networks: A Survey." International Journal of Automation and Computing 18, no. 4 (June 4, 2021): 503–20. http://dx.doi.org/10.1007/s11633-021-1302-3.

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AbstractSocial propagation denotes the spread phenomena directly correlated to the human world and society, which includes but is not limited to the diffusion of human epidemics, human-made malicious viruses, fake news, social innovation, viral marketing, etc. Simulation and optimization are two major themes in social propagation, where network-based simulation helps to analyze and understand the social contagion, and problem-oriented optimization is devoted to contain or improve the infection results. Though there have been many models and optimization techniques, the matter of concern is that the increasing complexity and scales of propagation processes continuously refresh the former conclusions. Recently, evolutionary computation (EC) shows its potential in alleviating the concerns by introducing an evolving and developing perspective. With this insight, this paper intends to develop a comprehensive view of how EC takes effect in social propagation. Taxonomy is provided for classifying the propagation problems, and the applications of EC in solving these problems are reviewed. Furthermore, some open issues of social propagation and the potential applications of EC are discussed. This paper contributes to recognizing the problems in application-oriented EC design and paves the way for the development of evolving propagation dynamics.

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WANI, Shabir Hussain, and Gulzar S. SANGHERA. "Genetic Engineering for Viral Disease Management in Plants." Notulae Scientia Biologicae 2, no. 1 (March 9, 2010): 20–28. http://dx.doi.org/10.15835/nsb213614.

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Viral diseases are a major threat to world agriculture and breeding resistant varieties against these viruses is one of the major challenge faced by plant virologists and biotechnologists. The development of the concept of pathogen derived resistance gave rise to strategies ranging from coat protein based interference of virus propagation to RNA mediated virus gene silencing. Much progress has been achieved in protecting plants against these RNA and DNA viruses. In this review, the most recent transgene based approaches for viral disease management in plants will be discussed.

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de Sessions, Paola Florez, Elena Dobrikova, and Matthias Gromeier. "Genetic Adaptation to Untranslated Region-Mediated Enterovirus Growth Deficits by Mutations in the Nonstructural Proteins 3AB and 3CD." Journal of Virology 81, no. 16 (May 30, 2007): 8396–405. http://dx.doi.org/10.1128/jvi.00321-07.

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ABSTRACT Both untranslated regions (UTRs) of plus-strand RNA virus genomes jointly control translation and replication of viral genomes. In the case of the Enterovirus genus of the Picornaviridae family, the 5′UTR consists of a cloverleaf-like terminus preceding the internal ribosomal entry site (IRES) and the 3′ terminus is composed of a structured 3′UTR and poly(A). The IRES and poly(A) have been implicated in translation control, and all UTR structures, in addition to cis-acting genetic elements mapping to the open reading frame, have been assigned roles in RNA replication. Viral UTRs are recognized by viral and host cell RNA-binding proteins that may codetermine genome stability, translation, plus- and minus-strand RNA replication, and scaffolding of viral replication complexes within host cell substructures. In this report, we describe experiments with coxsackie B viruses with a cell type-specific propagation deficit in Sk-N-Mc neuroblastoma cells conferred by the combination of a heterologous IRES and altered 3′UTR. Serial passage of these constructs in Sk-N-Mc cells yielded genetic adaptation by mutations within the viral nonstructural proteins 3A and 3C. Our data implicate 3A and/or 3C or their precursors 3AB and/or 3CD in a functional complex with the IRES and 3′UTR that drives viral propagation. Adaptation to neuroblastoma cells suggests an involvement of cell type-specific host factors or the host cell cytoplasmic milieu in this phenomenon.

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Lillestøl, Reidun, Peter Redder, Roger A. Garrett, and Kim Brügger. "A putative viral defence mechanism in archaeal cells." Archaea 2, no. 1 (2006): 59–72. http://dx.doi.org/10.1155/2006/542818.

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Clusters of regularly spaced direct repeats, separated by unconserved spacer sequences, are ubiquitous in archaeal chromosomes and occur in some plasmids. Some clusters constitute around 1% of chromosomal DNA. Similarly structured clusters, generally smaller, also occur in some bacterial chromosomes. Although early studies implicated these clusters in segregation/partition functions, recent evidence suggests that the spacer sequences derive from extrachromosomal elements, and, primarily, viruses. This has led to the proposal that the clusters provide a defence against viral propagation in cells, and that both the mode of inhibition of viral propagation and the mechanism of adding spacer-repeat units to clusters, are dependent on RNAs transcribed from the clusters. Moreover, the putative inhibitory apparatus (piRNA-based) may be evolutionarily related to the interference RNA systems (siRNA and miRNA), which are common in eukarya. Here, we analyze all the current data on archaeal repeat clusters and provide some new insights into their diverse structures, transcriptional properties and mode of structural development. The results are consistent with larger cluster transcripts being processed at the centers of the repeat sequences and being further trimmed by exonucleases to yield a dominant, intracellular RNA species, which corresponds approximately to the size of a spacer. Furthermore, analysis of the extensive clusters ofSulfolobus solfataricusstrains P1 and P2B provides support for the presence of a flanking sequence adjoining a cluster being a prerequisite for the incorporation of new spacer-repeat units, which occurs between the flanking sequence and the cluster. An archaeal database summarizing the data will be maintained at http://dac.molbio.ku.dk/dbs/SRSR/.

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Journal articles on the topic 'Propagation virale'

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