Relevant bibliographies by topics / Coxsackieviruses. Enterovirus

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  2. Dissertations / Theses
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  4. Book chapters

Academic literature on the topic 'Coxsackieviruses. Enterovirus'

Author: Grafiati
Published: 4 June 2021
Last updated: 2 February 2022

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Journal articles on the topic "Coxsackieviruses. Enterovirus"

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Romanenkova, N. I., N. R. Rozaeva, M. A. Bichurina, O. I. Kanaeva, I. G. Chkhyndzheriya, L. V. Shishkina, A. G. Madoyan, and N. V. Valdaitseva. "Epidemiological aspects of enterovirus infection in the Russian Federation during the period of 2018–2019." Journal Infectology 13, no. 1 (March 30, 2021): 108–16. http://dx.doi.org/10.22625/2072-6732-2021-13-1-108-116.

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Aim: Analysis of enterovirus infection morbidity and characteristics of the etiological agents of this infection on some territories of Russia in 2017.Materials and methods: We investigated 7858 samples of the biological material from the patients suffering from enterovirus infection. The isolation and identification of enteroviruses were conducted by virological and molecular methods.Results: The epidemic process and the clinical picture of enterovirus infection on different territories had some peculiarities. On some territories enterovirus meningitis was the predominant form of infection, on other territories enterovirus infection with exanthema prevailed. In Saint-Petersburg, Archangel and Saratov regions the percentage of enterovirus infection cases with the clinical picture of enterovirus meningitis was significantly higher than the percentage of enterovirus infection with exanthema. In the Komi Republic, Leningrad and Murmansk regions the percentage of infection with exanthema was statistically higher than the enterovirus meningitis portion. Enteroviruses of 30 serotypes were detected in the samples of patients suffering from enterovirus infection. We determined the etiology of sporadic and epidemic cases of enterovirus infection represented by different clinical forms. On some territories the epidemic foci of enterovirus infection among children were revealed. The etiological agents of enterovirus meningitis foci in Saint-Petersburg, Murmansk and Saratov regions were Coxsackievirus B5, Coxsackievirus B4 and Echovirus 30. The foci of enterovirus infection with exanthema in Archangel, Leningrad, Murmansk and Novgorod regions were caused by Coxsackieviruses A10, A16 and A6.Conclusion: The clinical forms of enterovirus infection on some territories were provoked by enteroviruses which dominated in the circulation on one or other territory. Enteroviruses of species B, mainly Echovirus 30, Echovirus 6 and Coxsackieviruses B1–6 were the etiological agents of enterovirus meningitis. The etiological factors of enterovirus infection with exanthema were Enteroviruses of species A, mainly Coxsackieviruses of different serotypes as well as Enterovirus 71.
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Paklonskaya, N. V., T. V. Amvrosieva, Y. A. Shilova, and E. P. Kishkurno. "Molecular epydemiology of enterovirus infection in the Republic of Belarus in 2016–2017." Proceedings of the National Academy of Sciences of Belarus, Medical series 16, no. 3 (September 16, 2019): 339–48. http://dx.doi.org/10.29235/1814-6023-2019-16-3-339-348.

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Enteroviruses are widespread human pathogens characterized by a high level of a genetic diversity. They cause different clinical forms of infection. The aim of the present study was to analyze the molecular epidemiology of enterovirus infection in the application to the structure of its clinical forms in 2016–2017.ECHO viruses predominated among patients with aseptic meningitis and were prevailing group of enteroviruses in 2016 (all ECHO viruses – 58%, including ECHO 9 – 26%, ECHO 6 –14%, ECHO 16 – 10%). In 2017, Coxsackieviruses prevailed (68%), that were including Coxsackievirus B5 (31%), Coxsackievirus B1, Coxsackievirus B4 and Coxsackievirus A6 (9% of each serotype). Coxsackieviruses were detected more frequently in patients with vesicular pharyngitis and unspecified enterovirus infection. The results of the molecular epidemiological analysis indicated that the prevalence of ECHO viruses in 2016 and Coxsackieviruses B in 2017 was due to the emergence of numerous new genovariants of these viruses.
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Romanenkova, N. I., L. N. Golitsyna, M. A. Bichurina, N. R. Rozaeva, O. I. Kanaeva, V. V. Zverev, D. V. Sozonov, et al. "Enterovirus infection morbidity and peculiarities of nonpolio enteroviruses circulation on some territories of Russia in 2017." Journal Infectology 10, no. 4 (December 30, 2018): 124–33. http://dx.doi.org/10.22625/2072-6732-2018-10-4-124-133.

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Aim: Characteristics of enterovirus infection morbidity and study of peculiarities of enterovirus circulation on some territories of Russia in 2017. Materials and methods: We investigated more than 5000 samples from the patients with enterovirus infection. The isolation and identification of enteroviruses were conducted by virological method and by partial sequencing of the genome region VP1. Phylogenic trees were constructed according to the method of Bayesian Monte Carlo Markov Chain. Results: Epidemic process and clinical picture of enterovirus infection were not the same on different territories. Peculiarities of the circulation of different types of enteroviruses on the territories were also different. In Saratov region 65% of cases were represented by enterovirus meningitis. In Murmansk region and in the Komi Republic enterovirus infection with exanthema prevailed, 95% and 60% correspondingly. In Saratov region enterovirus ECHO18 was the etiological agent of enterovirus meningitis. In Murmansk region and in the Komi Republic the cases were connected mainly with Coxsackieviruses A6. The strains of enterovirus ECHO18 were distributed to three clusters. The strains which provoked enterovirus meningitis in Saratov region belonged to cluster 3, they were formed separately from other strains of this enterovirus type and differed from the stains of ECHO18 which circulated in the North-West of Russia. The strains of Coxsackieviruses A6 identified in the North-West of Russia belonged to three sub-genotypes 5, 6, 8 of pandemic genotype of CoxsackievirusesA6. The majority of the strains belonged to sub-genotypes 6 and 8 which in 2017 dominated in the structure of Coxsackieviruses A6 in the North-West of Russia and in Russia. Conclusion: Epidemic peaks of enterovirus infection represented by different clinical forms of the disease were provoked by different types of enteroviruses. Enterovirus ECHO18 was the etiological agent of enterovirus meningitis. The main etiological factors of enterovirus infection with exanthema were Coxsackieviruses A6 of different sub-genotypes.
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Richter, Jan, Dana Koptides, Christina Tryfonos, and Christina Christodoulou. "Molecular typing of enteroviruses associated with viral meningitis in Cyprus, 2000–2002." Journal of Medical Microbiology 55, no. 8 (August 1, 2006): 1035–41. http://dx.doi.org/10.1099/jmm.0.46447-0.

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Human enteroviruses are responsible for a wide spectrum of clinical diseases affecting many different organ systems. Although infection is usually asymptomatic, infections of the central nervous system manifested as meningitis or encephalitis can pose a serious public health problem, especially during outbreaks. In this study, samples from 218 patients diagnosed with enteroviral meningitis between January 2000 and December 2002 were analysed in order to assess the epidemiology of human enteroviruses as a cause of viral meningitis in Cyprus. A new typing strategy, based on partial sequencing of the 5′ non-coding region (5′NCR), prediction of type, and selection of type-specific primers for sensitive VP1 PCR amplification, was developed. As clustering in the 5′NCR was concordant with clustering in the VP1 region, quick and reliable typing by VP1 sequencing was achieved without virus isolation in cell culture. The most frequent enterovirus serotypes identified were Human echovirus 30 (55.5 %), Human echovirus 13 (15.1 %), Human echovirus 6 (13.8 %) and Human echovirus 9 (8.3 %). Human coxsackieviruses B2, B1 and B5, Human echovirus 4, Human enterovirus 71 and Human coxsackievirus A6 represented rather rare serotypes. This is the first molecular epidemiological study of enterovirus meningitis in Cyprus. Serotype distribution corresponded basically with observations in other European countries, suggesting the spread of enteroviruses by tourism.
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Rigonan, Alma S., Linda Mann, and Tasnee Chonmaitree. "Use of Monoclonal Antibodies To Identify Serotypes of Enterovirus Isolates." Journal of Clinical Microbiology 36, no. 7 (1998): 1877–81. http://dx.doi.org/10.1128/jcm.36.7.1877-1881.1998.

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Nonpoliovirus enteroviruses cause a variety of diseases that are common in young children and adults. The “gold standard” for laboratory diagnosis of enteroviruses is cell culture isolation, followed by serotype identification by neutralization assay. These procedures are time-consuming and expensive. Rapid serotype identification of enteroviruses is important in differentiating nonpoliovirus enterovirus pathogens from vaccine strain polioviruses that can be shed for some time after vaccination. In the present investigation, we evaluated a rapid method for serotype identification of enteroviruses by indirect immunofluorescence assay (IFA) using commercially available monoclonal antibodies for polioviruses, coxsackieviruses type B, and six serotypes of commonly circulating echoviruses. Of 291 isolates of enteroviruses included in the study, 95 were polioviruses and 196 were nonpoliovirus enteroviruses. Two hundred thirty-four of these (38 polioviruses and 196 nonpoliovirus enteroviruses) were consecutively grown in the laboratory over a 5-year period. IFA identified the serotypes of 74% of the consecutive isolates and 71% of all enterovirus isolates by yielding a positive staining result. The levels of agreement in the identification of the enterovirus group between IFA and neutralization tests were 92% for consecutively grown isolates and 85% for all enterovirus isolates. The sensitivity of the IFA for the detection of viruses for which specific monoclonal antibodies were applied was 73% for polioviruses, 85% for coxsackieviruses type B, and 94% for echoviruses. Specificity was near 100% for polioviruses and coxsackieviruses type B and 94% for echoviruses. We conclude that IFA can be helpful as a preliminary test for serotype identification of enteroviruses. The results are most accurate when the test identifies the isolate as a poliovirus.
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Wells, Alexandra I., and Carolyn B. Coyne. "Enteroviruses: A Gut-Wrenching Game of Entry, Detection, and Evasion." Viruses 11, no. 5 (May 21, 2019): 460. http://dx.doi.org/10.3390/v11050460.

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Enteroviruses are a major source of human disease, particularly in neonates and young children where infections can range from acute, self-limited febrile illness to meningitis, endocarditis, hepatitis, and acute flaccid myelitis. The enterovirus genus includes poliovirus, coxsackieviruses, echoviruses, enterovirus 71, and enterovirus D68. Enteroviruses primarily infect by the fecal–oral route and target the gastrointestinal epithelium early during their life cycles. In addition, spread via the respiratory tract is possible and some enteroviruses such as enterovirus D68 are preferentially spread via this route. Once internalized, enteroviruses are detected by intracellular proteins that recognize common viral features and trigger antiviral innate immune signaling. However, co-evolution of enteroviruses with humans has allowed them to develop strategies to evade detection or disrupt signaling. In this review, we will discuss how enteroviruses infect the gastrointestinal tract, the mechanisms by which cells detect enterovirus infections, and the strategies enteroviruses use to escape this detection.
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Weinzierl, Andreas O., Despina Rudolf, Dominik Maurer, Dorothee Wernet, Hans-Georg Rammensee, Stefan Stevanović, and Karin Klingel. "Identification of HLA-A*01- and HLA-A*02-restricted CD8+ T-cell epitopes shared among group B enteroviruses." Journal of General Virology 89, no. 9 (September 1, 2008): 2090–97. http://dx.doi.org/10.1099/vir.0.2008/000711-0.

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Acute enteroviral infections ranging from meningitis, pancreatitis to myocarditis are common and normally well controlled by the host immune system comprising virus-specific CD8+ cytotoxic T lymphocytes (CTL). However, in some patients enteroviruses and especially coxsackieviruses of group B are capable of inducing severe chronic forms of diseases such as chronic myocarditis. Currently, it is not known whether divergences in the CTL-related immune response may contribute to the different outcome and course of enterovirus myocarditis. A pre-requisite for the study of CTL reactions in patients with acute and chronic myocarditis is the identification of CTL epitopes. In order to define dominant enterovirus CTL epitopes, we have screened, by using gamma interferon (IFN-γ) ELISPOT, 62 HLA-A*01- and 59 HLA-A*02-positive healthy blood donors for pre-existing CTL reactions against 12 HLA-A*01 and 20 HLA-A*02 predicted CTL epitopes derived from coxsackieviruses of group B. Positive CTL reactions were verified by FACS analysis in a combined major histocompatibility complex-tetramer IFN-γ staining. A total of 14.8 % of all donors reacted against one of the three identified epitopes MLDGHLIAFDY, YGDDVIASY or GIIYIIYKL. The HLA-A*02-restricted epitope ILMNDQEVGV was recognized by 25 % of all tested blood donors. For this peptide, we could demonstrate specific granzyme B secretion, a strong cytolytic potential and endogenous processing. All four epitopes were homologous in 36–92 % of group B enteroviruses, providing a strong basis for monitoring the divergence of T-cell-based immune responses in enterovirus-induced acute and chronic diseases.
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Lukashev, Alexander N., Elena Yu Shumilina, Ilya S. Belalov, Olga E. Ivanova, Tatiana P. Eremeeva, Vadim I. Reznik, O. E. Trotsenko, Jan Felix Drexler, and Christian Drosten. "Recombination strategies and evolutionary dynamics of the Human enterovirus A global gene pool." Journal of General Virology 95, no. 4 (April 1, 2014): 868–73. http://dx.doi.org/10.1099/vir.0.060004-0.

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We analysed natural recombination in 79 Human enterovirus A strains representing 13 serotypes by sequencing of VP1, 2C and 3D genome regions. The half-life of a non-recombinant tree node in coxsackieviruses 2, 4 and 10 was only 3.5 years, and never more than 9 years. All coxsackieviruses that differed by more than 7 % of the nucleotide sequence in any genome region were recombinants relative to each other. Enterovirus 71 (EV71), on the contrary, displayed remarkable genetic stability. Three major EV71 clades were stable for 19–29 years, with a half-life of non-recombinant viruses between 13 and 18.5 years in different clades. Only five EV71 strains out of over 150 recently acquired non-structural genome regions from coxsackieviruses, while none of 80 contemporary coxsackieviruses had non-structural genes transferred from the three EV71 clades. In contrast to earlier observations, recombination between VP1 and 2C genome regions was not more frequent than between 2C and 3D regions.
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Duijsings, Daniël, Els Wessels, Sjenet E. van Emst-de Vries, Willem J. G. Melchers, Peter H. G. M. Willems, and Frank J. M. van Kuppeveld. "Reduction of phospholipase D activity during coxsackievirus infection." Journal of General Virology 88, no. 11 (November 1, 2007): 3027–30. http://dx.doi.org/10.1099/vir.0.83169-0.

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During enterovirus infection, host cell membranes are rigorously rearranged and modified. One ubiquitously expressed lipid-modifying enzyme that might contribute to these alterations is phospholipase D (PLD). Here, we investigated PLD activity in coxsackievirus-infected cells. We show that PLD activity is not required for efficient coxsackievirus RNA replication. Instead, PLD activity rapidly decreased upon infection and upon ectopic expression of the viral 3A protein, which inhibits the PLD activator ADP-ribosylation factor 1. However, similar decreases were observed during infection with coxsackieviruses carrying defective mutant 3A proteins. Possible causes for the reduction of PLD activity and the biological consequences are discussed.
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Pons-Salort, Margarita, and Nicholas C. Grassly. "Serotype-specific immunity explains the incidence of diseases caused by human enteroviruses." Science 361, no. 6404 (August 23, 2018): 800–803. http://dx.doi.org/10.1126/science.aat6777.

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Human enteroviruses are a major cause of neurological and other diseases. More than 100 serotypes are known that exhibit unexplained complex patterns of incidence, from regular cycles to more irregular patterns, and new emergences. Using 15 years of surveillance data from Japan (2000–2014) and a stochastic transmission model with accurate demography, we show that acquired serotype-specific immunity can explain the diverse patterns of 18 of the 20 most common serotypes (including Coxsackieviruses, Echoviruses, and Enterovirus-A71). The remaining two serotypes required a change in viral characteristics, including an increase in pathogenicity for Coxsackievirus-A6, which is consistent with its recent global rise in incidence. On the basis of our findings, we are able to predict outbreaks 2 years ahead of time (2015–2016). These results have implications for the impact of vaccines under development.
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Dissertations / Theses on the topic "Coxsackieviruses. Enterovirus"

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Hindersson, Maria. "Coxsackie B virus pathogenesis in mice /." Stockholm : Karolinska institutet, 2006. http://diss.kib.ki.se/2006/20060608hind/.

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Lau, Ming-ho, and 劉明昊. "Risk factors of hand foot mouth diseases outbreaks in kindergartens inHong Kong." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B42994901.

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Lau, Ming-ho. "Risk factors of hand foot mouth diseases outbreaks in kindergartens in Hong Kong." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B42994901.

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Triantafilou, Martha. "Interactions of coxsackievirus A9 with cellular receptors." Thesis, University of Essex, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.285856.

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Mirza, Momina. "Characterization of the cellular receptor for coxsackievirus and adenovirus /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-889-4/.

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Sävneby, Anna. "Reverse genetic studies of Enterovirus replication." Doctoral thesis, Linnéuniversitetet, Institutionen för kemi och biomedicin (KOB), 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-41636.

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Enteroviruses belong to the Picornaviridae family and are small icosahedral viruses with RNA genomes of positive polarity, containing a single open reading frame. They mostly cause mild or asymptomatic infections, but also a wide array of diseases including: poliomyelitis, encephalitis, gastroenteritis, aseptic meningitis, myocarditis, hand-foot-and-mouth disease, hepatitis and respiratory diseases, ranging from severe infections to the common cold. The projects described in this thesis have been carried out through reverse genetic studies of Enterovirus B and Rhinovirus C.                   In Papers I and II, a cassette vector was used to study recombination and translation of the RNA genome. It was found that the non-structural coding region could replicate when combined with the structural protein-coding region of other viruses of the same species. Furthermore, the genome could be translated and replicated without the presence of the structural protein-coding region. Moreover, it was found that when two additional nucleotides were introduced, shifting the reading frame, the virus could revert to the original reading frame, restoring efficient replication. In Paper III, a vector containing the genome of echovirus 5 was altered to produce an authentic 5’end of the in vitro transcribed RNA, which increased efficiency of replication initiation 20 times. This result is important, as it may lead to more efficient oncolytic virotherapy. An authentic 5’end was further used in Paper IV, where replication of Rhinovirus C in cell lines was attempted. Although passaging of the virus was unsuccessful, the genome was replicated and cytopathic effect induced after transfection. The restriction of efficient replication was therefore hypothesized to lie in the attachment and entry stages of the replication cycle. In Paper V, a cytolytic virus was found to have almost 10 times larger impact on gene expression of the host cell than a non-cytolytic variant. Furthermore, the lytic virus was found to build up inside the host cell, while the non-cytolytic virus was efficiently released.                   As a whole, this thesis has contributed to a deeper understanding of replication of enteroviruses, which may prove important in development of novel vaccines, antiviral agents and oncolytic virotherapies.
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Wehbe, Michel. "Etude de l’activité de réplication des formes de Coxsackievirus B3 complètes et tronquées dans la région 5’non codante dans un modèle de cardiomyocytes humains primaires en culture." Thesis, Reims, 2016. http://www.theses.fr/2016REIMS042.

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Les Entérovirus humains du groupe B (EV-B) et plus spécifiquement les virus Coxsackie B sont considérés comme une cause majeure des myocardites infectieuses aigues et chroniques dont 10% peuvent évoluer vers la cardiomyopathie dilatée (CMD). Les mécanismes moléculaires viraux impliqués dans la progression de la myocardite aiguë vers le stade de la CMD ne sont pas élucidés.L’analyse par séquençage NGS a montré chez 8 (33%) des 24 patients atteints de CMD inexpliquée l’existence de populations majoritaires tronquées de 19 à 50 nucléotides associées à des formes virales minoritaires complètes. La proportion de populations tronquées s’est révélée négativement corrélée au ratio ARN+/ARN- et à la charge virale. Des études immuno-histologiques et par hybridation in situ des tissus cardiaques ont montré que le clivage de la dystrophine était uniquement retrouvé dans les cardiomyocytes infectés par les EV-B. Pour étudier les activités de réplication des populations d’EV-B persistants, un réplicon (CVB3-emGFP) a été généré à partir d’une souche cardiotrope (CV-B3/28). La transfection d’ARN de synthèse complets et tronqués (d50) dans des cultures de cardiomyocytes humains primaires a mis en évidence des mécanismes de recombinaison et/ou de trans-complémentation entre ces 2 formes virales induisant de faibles activités de réplication.Nos résultats démontrent l’existence de mécanismes de coopération moléculaire entre des populations d’EV-B tronquées et complètes qui pourraient expliquer la mise en place du mécanisme de persistance virale observée au cours de la phase clinique de CMD. Ces résultats pourraient contribuer au développement de nouvelles stratégies thérapeutiques pour prévenir et traiter les infections cardiaques à EV-B
Enteroviruses group B (EV-B) and more specifically Coxsackievirus B are recognized as major causes of acute and chronic infectious myocarditis, which 10% may progress towards dilated cardiomyopathy (DCM). Viral molecular mechanisms involved in the progression from acute myocarditis to the clinical stage of DCM remain unknown.Deep sequencing analysis showed in 8 (33%) of 24 unexplained DCM patients the existence of major CVB3 populations with deletions of 19 to 50 nucleotides associated with a minority of complete viral forms. The proportion of deleted viral populations was negatively correlated with RNA+/RNA- ratio and the viral load levels. Immuno-histological and in situ hybridization assays of DCM cardiac tissues demonstrated that the cleavage of dystrophin was found only in cardiomyocytes infected with EV-B. To study the replication activities of persistent EV-B populations, a replicon (CVB3-emGFP) was generated from a cardiotropic strain (CV-B3/28). Transfection of synthesized complete and truncated (d50) viral RNAs in primary human cardiomyocytes cultures revealed mechanisms of recombination and / or trans-complementation between these two viral forms inducing low replication activities.In conclusions, our original results demonstrated the existence of new molecular mechanisms of cooperation between EV-B deleted and complete viral populations that could explain the development of a viral persistence mechanism observed during the clinical phase of DCM. These findings may contribute to the development of new therapeutic strategies to prevent and treat persistent heart EV-B infections
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Skog, Oskar. "Effects of Enterovirus Infection on Innate Immunity and Beta Cell Function in Human Islets of Langerhans." Doctoral thesis, Uppsala universitet, Klinisk immunologi, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-172586.

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This thesis focuses on enteroviral effects on human pancreatic islets. Most knowledge of viral effects on host cells relies on studies of immortalized cell lines or animal models. The islets represent a fundamentally different and less well studied cellular host. Also, enterovirus has been implicated in the etiology of type 1 diabetes (T1D). We show that when enterovirus replicates in human islets it activates innate immunity genes and induces secretion of the chemokines MCP-1 and IP-10. An important difference in activation of innate immunity by replicating EV and synthetic dsRNA is suggested, since the chemokine secretion induced by EV infection but not by dsRNA is reduced by female sex hormone. We also demonstrate a direct antiviral effect of nicotinamide, and even though this substance failed to prevent T1D in a large-scale study, this finding could have implications for the treatment/prevention of virus- and/or immune-mediated disease. We also had access to human pancreata from two organ donors with recent onset T1D and several donors with T1D-related autoantibodies, which gave us the opportunity to study ongoing pathogenic processes at and before the onset of T1D. Despite this, we could neither confirm nor reject the hypothesis that EV is involved in T1D development. Several observations, such as ultrastructural remodeling of the beta cell, activation of innate immunity, and immunopositivity to EV capsid protein 1, supported an ongoing virus infection, but direct evidence is still lacking. An interesting finding in the donors with recent onset T1D was that the islets were positively stained for insulin, but did not secrete insulin in response to glucose-stimulation. A similar effect was observed in EV-infected islets in vitro; EV destroyed islet function and insulin gene expression, but the islets still stained positive for insulin. This may be indicative of that a functional block in addition to beta cell destruction is involved in T1D pathogenesis. In conclusion, these studies of EV in isolated human islets in vitro support that this virus can cause T1D in vivo, but future studies will have to show if and how frequently this happens.
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Peng, Jian Hong. "Immunological and molecular relationship of swine vesicular disease virus with coxsackievirus B5 and other enteroviruses of pigs." Thesis, University of Hertfordshire, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283405.

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Sane, Famara. "Infection à Coxsackievirus B4 et prévention." Phd thesis, Université du Droit et de la Santé - Lille II, 2012. http://tel.archives-ouvertes.fr/tel-00793386.

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Le diabète de type 1 (DT1) est une maladie chronique multifactorielle. Les infections entérovirales, en particulier à Coxsackievirus du groupe B (CVB), et notamment CVB4, transmises par voie digestive, constituent le facteur de risque le plus souvent évoqué dans la littérature. Plusieurs mécanismes physiopathologiques sont proposés pour expliquer cette relation entre CVB4 et diabète de type 1. Il s'agit, entre autres, du tropisme préférentiel de CVB4 pour les ilots et les cellules β pancréatiques et l'inflammation qui s'ensuit, de la persistance du virus au niveau des cellules infectées qui pourrait constituer un facteur déterminant dans le processus d'altération des cellules endocrines, de l'exacerbation possible de l'infection par des d'anticorps facilitateurs ou encore du mimétisme moléculaire entre les auto-antigènes et les antigènes viraux. Par ailleurs des auteurs ont montré que la cause de la déplétion des cellules β chez des souris infectées par la souche diabétogénique CVB4E2 est un défaut de régénération plutôt qu'une destruction directe de ces cellules par le virus. La présence de constituants entéroviraux dans les cellules ductales du pancréas de patients diabétiques a été observée. Le diabète de type 1, qui serait l'expression finale d'un long processus, survient généralement chez des sujets jeunes, c'est pourquoi l'hypothèse que le tissu pancréatique jeune serait plus permissif aux infections à CVB4 n'est pas exclue. La prévention des infections virales reste le meilleur moyen de protéger les individus contre les maladies qu'elles provoquent. Un intérêt particulier est aujourd'hui accordé à la mise en évidences et à la caractérisation d'inhibiteurs antiviraux à large spectre. L'absence d'allaitement maternel est associé à un risque plus élevé de diabète de type 1, mais la nature du ou des facteurs du lait conférant une protection est mal connue, et l'activité anti-CVB4 du lait maternel n'a pas été étudiée jusqu'à présent. Objectifs : Nous avons émis l'hypothèse que CVB4 pouvait infecter des cellules humaines précurseurs de cellules endocrines, impliquées dans la régénération des îlots. L'infection de ces cellules par CVB4E2 et ses conséquences ont été étudiées ; nous avons utilisé des cellules humaines précurseurs canalaires primitives et la lignée continue de cellules Panc-1, dont la différenciation in vitro est possible. La permissivité au CVB4 du tissu pancréatique selon l'âge a été étudiée ex vivo chez le rat et l'existence d'inhibiteurs antiviraux à large spectre est notamment explorée dans l'intestin de souris. L'activité anti-CVB4 du lait maternel susceptible de protéger, à un âge critique, le jeune enfant vis-à-vis d'un virus diabétogène a été étudiée in vitro et l'hypothèse que le lait humain pourrait prévenir le déclenchement du DT1 chez la souris NOD a également été évaluée in vivo.
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Books on the topic "Coxsackieviruses. Enterovirus"

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Group B coxsackieviruses. Berlin: Springer, 2008.

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Tracy, S. The Coxsackie B Viruses. Edited by S. Tracy. SPRINGER-VERLAG, 1997.

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Book chapters on the topic "Coxsackieviruses. Enterovirus"

1

Kandolf, Reinhard. "The Impact of Recombinant DNA Technology on the Study of Enterovirus Heart Disease." In Coxsackieviruses, 293–318. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4757-0247-7_17.

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Kapsenberg, Jacoba G. "Picornaviridae: The Enteroviruses (Polioviruses, Coxsackieviruses, Echoviruses)." In Laboratory Diagnosis of Infectious Diseases Principles and Practice, 692–722. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4612-3900-0_36.

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Oberste, M. Steven, and Susan I. Gerber. "Enteroviruses and Parechoviruses: Echoviruses, Coxsackieviruses, and Others." In Viral Infections of Humans, 225–52. Boston, MA: Springer US, 2014. http://dx.doi.org/10.1007/978-1-4899-7448-8_11.

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Werner, S., H. Schönke, W. Klump, P. H. Hofschneider, and R. Kandolf. "Generation of Enterovirus Group-Specific Antisera Using Bacterially Synthesized Coxsackievirus B3 Proteins." In New Concepts in Viral Heart Disease, 125–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73610-0_12.

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Mall, G., K. Klingel, M. Albrecht, M. Seemann, T. Mandel, and R. Kandolf. "Natural History of Enterovirus Persistence in the Murine Model of Coxsackievirus-Induced Myocarditis: A Quantitative In Situ Hybridization and Immunohistochemistry Study." In Idiopathic Dilated Cardiomyopathy, 294–300. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77891-9_26.

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Jung, Chaeyun, Yonghyun Park, Seunghui Han, and Taeseon Yoon. "Analyzing the Genomes of Coxsackievirus A16 and Enterovirus 71 in Relation to Hand, Foot and Mouth Disease(HFMD) Using Apriori Algorithm, Decision Tree and Support Vector Machine (SVM)." In Intelligent Computing Theories and Methodologies, 539–45. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-22180-9_53.

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Modlin, John F. "Enteroviruses: Coxsackieviruses, Echoviruses, and Newer Enteroviruses." In Principles and Practice of Pediatric Infectious Disease, 1149–57. Elsevier, 2008. http://dx.doi.org/10.1016/b978-0-7020-3468-8.50243-1.

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Romero, José R., and John F. Modlin. "Coxsackieviruses, Echoviruses, and Numbered Enteroviruses." In Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases, 2080–90. Elsevier, 2015. http://dx.doi.org/10.1016/b978-1-4557-4801-3.00174-0.

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MODLIN, JOHN F. "Coxsackieviruses, Echoviruses, Newer Enteroviruses, and Parechoviruses." In Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases, 2353–65. Elsevier, 2010. http://dx.doi.org/10.1016/b978-0-443-06839-3.00172-7.

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