Relevant bibliographies by topics / Flavivirus

Academic literature on the topic 'Flavivirus'

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Published: 4 June 2021
Last updated: 25 May 2024

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Journal articles on the topic "Flavivirus"

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Qiu, Yang, Yan-Peng Xu, Miao Wang, Meng Miao, Hui Zhou, Jiuyue Xu, Jing Kong, et al. "Flavivirus induces and antagonizes antiviral RNA interference in both mammals and mosquitoes." Science Advances 6, no. 6 (February 2020): eaax7989. http://dx.doi.org/10.1126/sciadv.aax7989.

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Mosquito-borne flaviviruses infect both mammals and mosquitoes. RNA interference (RNAi) has been demonstrated as an anti-flavivirus mechanism in mosquitoes; however, whether and how flaviviruses induce and antagonize RNAi-mediated antiviral immunity in mammals remains unknown. We show that the nonstructural protein NS2A of dengue virus-2 (DENV2) act as a viral suppressor of RNAi (VSR). When NS2A-mediated RNAi suppression was disabled, the resulting mutant DENV2 induced Dicer-dependent production of abundant DENV2-derived siRNAs in differentiated mammalian cells. VSR-disabled DENV2 showed severe replication defects in mosquito and mammalian cells and in mice that were rescued by RNAi deficiency. Moreover, NS2As of multiple flaviviruses act as VSRs in vitro and during viral infection in both organisms. Overall, our findings demonstrate that antiviral RNAi can be induced by flavivirus, while flavivirus uses NS2A as a bona fide VSR to evade RNAi in mammals and mosquitoes, highlighting the importance of RNAi in flaviviral vector-host life cycles.
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Wee, Sheena, Asfa Alli-Shaik, Relus Kek, Hannah L. F. Swa, Wei-Ping Tien, Vanessa W. Lim, Yee-Sin Leo, Lee-Ching Ng, Hapuarachchige C. Hapuarachchi, and Jayantha Gunaratne. "Multiplex targeted mass spectrometry assay for one-shot flavivirus diagnosis." Proceedings of the National Academy of Sciences 116, no. 14 (March 18, 2019): 6754–59. http://dx.doi.org/10.1073/pnas.1817867116.

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Targeted proteomic mass spectrometry is emerging as a salient clinical diagnostic tool to track protein biomarkers. However, its strong analytical properties have not been exploited in the diagnosis and typing of flaviviruses. Here, we report the development of a sensitive and specific single-shot robust assay for flavivirus typing and diagnosis using targeted mass spectrometry technology. Our flavivirus parallel reaction monitoring assay (fvPRM) has the ability to track secreted flaviviral nonstructural protein 1 (NS1) over a broad diagnostic and typing window with high sensitivity, specificity, extendibility, and multiplexing capability. These features, pivotal and pertinent to efficient response toward flavivirus outbreaks, including newly emerging flavivirus strains, circumvent the limitations of current diagnostic assays.fvPRM thus carries high potential in positioning itself as a forerunner in delivering early and accurate diagnosis for disease management.
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van den Elsen, Kaïn, Jun Ping Quek, and Dahai Luo. "Molecular Insights into the Flavivirus Replication Complex." Viruses 13, no. 6 (May 21, 2021): 956. http://dx.doi.org/10.3390/v13060956.

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Flaviviruses are vector-borne RNA viruses, many of which are clinically relevant human viral pathogens, such as dengue, Zika, Japanese encephalitis, West Nile and yellow fever viruses. Millions of people are infected with these viruses around the world each year. Vaccines are only available for some members of this large virus family, and there are no effective antiviral drugs to treat flavivirus infections. The unmet need for vaccines and therapies against these flaviviral infections drives research towards a better understanding of the epidemiology, biology and immunology of flaviviruses. In this review, we discuss the basic biology of the flavivirus replication process and focus on the molecular aspects of viral genome replication. Within the virus-induced intracellular membranous compartments, flaviviral RNA genome replication takes place, starting from viral poly protein expression and processing to the assembly of the virus RNA replication complex, followed by the delivery of the progeny viral RNA to the viral particle assembly sites. We attempt to update the latest understanding of the key molecular events during this process and highlight knowledge gaps for future studies.
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Wu, Bingan, Zhongtian Qi, and Xijing Qian. "Recent Advancements in Mosquito-Borne Flavivirus Vaccine Development." Viruses 15, no. 4 (March 23, 2023): 813. http://dx.doi.org/10.3390/v15040813.

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Lately, the global incidence of flavivirus infection has been increasing dramatically and presents formidable challenges for public health systems around the world. Most clinically significant flaviviruses are mosquito-borne, such as the four serotypes of dengue virus, Zika virus, West Nile virus, Japanese encephalitis virus and yellow fever virus. Until now, no effective antiflaviviral drugs are available to fight flaviviral infection; thus, a highly immunogenic vaccine would be the most effective weapon to control the diseases. In recent years, flavivirus vaccine research has made major breakthroughs with several vaccine candidates showing encouraging results in preclinical and clinical trials. This review summarizes the current advancement, safety, efficacy, advantages and disadvantages of vaccines against mosquito-borne flaviviruses posing significant threats to human health.
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Heinz, Franz X., and Karin Stiasny. "Flaviviruses and flavivirus vaccines." Vaccine 30, no. 29 (June 2012): 4301–6. http://dx.doi.org/10.1016/j.vaccine.2011.09.114.

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Liao, Ching-Len, Yi-Ling Lin, Bi-Ching Wu, Chang-Huei Tsao, Mei-Chuan Wang, Chiu-I. Liu, Yue-Ling Huang, Jui-Hui Chen, Jia-Pey Wang, and Li-Kuang Chen. "Salicylates Inhibit Flavivirus Replication Independently of Blocking Nuclear Factor Kappa B Activation." Journal of Virology 75, no. 17 (September 1, 2001): 7828–39. http://dx.doi.org/10.1128/jvi.75.17.7828-7839.2001.

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ABSTRACT Flaviviruses comprise a positive-sense RNA genome that replicates exclusively in the cytoplasm of infected cells. Whether flaviviruses require an activated nuclear factor(s) to complete their life cycle and trigger apoptosis in infected cells remains elusive. Flavivirus infections quickly activate nuclear factor kappa B (NF-κB), and salicylates have been shown to inhibit NF-κB activation. In this study, we investigated whether salicylates suppress flavivirus replication and virus-induced apoptosis in cultured cells. In a dose-dependent inhibition, we found salicylates within a range of 1 to 5 mM not only restricted flavivirus replication but also abrogated flavivirus-triggered apoptosis. However, flavivirus replication was not affected by a specific NF-κB peptide inhibitor, SN50, and a proteosome inhibitor, lactacystin. Flaviviruses also replicated and triggered apoptosis in cells stably expressing IκBα-ΔN, a dominant-negative mutant that antagonizes NF-κB activation, as readily as in wild-type BHK-21 cells, suggesting that NF-κB activation is not essential for either flavivirus replication or flavivirus-induced apoptosis. Salicylates still diminished flavivirus replication and blocked apoptosis in the same IκBα-ΔN cells. This inhibition of flaviviruses by salicylates could be partially reversed by a specific p38 mitogen-activated protein (MAP) kinase inhibitor, SB203580. Together, these results show that the mechanism by which salicylates suppress flavivirus infection may involve p38 MAP kinase activity but is independent of blocking the NF-κB pathway.
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Habarugira, Gervais, Jasmin Moran, Jessica J. Harrison, Sally R. Isberg, Jody Hobson-Peters, Roy A. Hall, and Helle Bielefeldt-Ohmann. "Evidence of Infection with Zoonotic Mosquito-Borne Flaviviruses in Saltwater Crocodiles (Crocodylus porosus) in Northern Australia." Viruses 14, no. 5 (May 21, 2022): 1106. http://dx.doi.org/10.3390/v14051106.

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The risk of flavivirus infections among the crocodilian species was not recognised until West Nile virus (WNV) was introduced into the Americas. The first outbreaks caused death and substantial economic losses in the alligator farming industry. Several other WNV disease episodes have been reported in crocodilians in other parts of the world, including Australia and Africa. Considering that WNV shares vectors with other flaviviruses, crocodilians are highly likely to also be exposed to flaviviruses other than WNV. A serological survey for flaviviral infections was conducted on saltwater crocodiles (Crocodylus porosus) at farms in the Northern Territory, Australia. Five hundred serum samples, collected from three crocodile farms, were screened using a pan-flavivirus-specific blocking ELISA. The screening revealed that 26% (n = 130/500) of the animals had antibodies to flaviviruses. Of these, 31.5% had neutralising antibodies to WNVKUN (Kunjin strain), while 1.5% had neutralising antibodies to another important flavivirus pathogen, Murray Valley encephalitis virus (MVEV). Of the other flaviviruses tested for, Fitzroy River virus (FRV) was the most frequent (58.5%) in which virus neutralising antibodies were detected. Our data indicate that farmed crocodiles in the Northern Territory are exposed to a range of potentially zoonotic flaviviruses, in addition to WNVKUN. While these flaviviruses do not cause any known diseases in crocodiles, there is a need to investigate whether infected saltwater crocodiles can develop a viremia to sustain the transmission cycle or farmed crocodilians can be used as sentinels to monitor the dynamics of arboviral infections in tropical areas.
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Fontoura, Marina Alves, Rebeca Fróes Rocha, and Rafael Elias Marques. "Neutrophil Recruitment and Participation in Severe Diseases Caused by Flavivirus Infection." Life 11, no. 7 (July 20, 2021): 717. http://dx.doi.org/10.3390/life11070717.

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Neutrophils are first-line responders to infections and are recruited to target tissues through the action of chemoattractant molecules, such as chemokines. Neutrophils are crucial for the control of bacterial and fungal infections, but their role in the context of viral infections has been understudied. Flaviviruses are important human viral pathogens transmitted by arthropods. Infection with a flavivirus may result in a variety of complex disease manifestations, including hemorrhagic fever, encephalitis or congenital malformations. Our understanding of flaviviral diseases is incomplete, and so is the role of neutrophils in such diseases. Here we present a comprehensive overview on the participation of neutrophils in severe disease forms evolving from flavivirus infection, focusing on the role of chemokines and their receptors as main drivers of neutrophil function. Neutrophil activation during viral infection was shown to interfere in viral replication through effector functions, but the resulting inflammation is significant and may be detrimental to the host. For congenital infections in humans, neutrophil recruitment mediated by CXCL8 would be catastrophic. Evidence suggests that control of neutrophil recruitment to flavivirus-infected tissues may reduce immunopathology in experimental models and patients, with minimal loss to viral clearance. Further investigation on the roles of neutrophils in flaviviral infections may reveal unappreciated functions of this leukocyte population while increasing our understanding of flaviviral disease pathogenesis in its multiple forms.
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Blahove, Maria Raisa, and James Richard Carter. "Flavivirus Persistence in Wildlife Populations." Viruses 13, no. 10 (October 18, 2021): 2099. http://dx.doi.org/10.3390/v13102099.

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A substantial number of humans are at risk for infection by vector-borne flaviviruses, resulting in considerable morbidity and mortality worldwide. These viruses also infect wildlife at a considerable rate, persistently cycling between ticks/mosquitoes and small mammals and reptiles and non-human primates and humans. Substantially increasing evidence of viral persistence in wildlife continues to be reported. In addition to in humans, viral persistence has been shown to establish in mammalian, reptile, arachnid, and mosquito systems, as well as insect cell lines. Although a considerable amount of research has centered on the potential roles of defective virus particles, autophagy and/or apoptosis-induced evasion of the immune response, and the precise mechanism of these features in flavivirus persistence have yet to be elucidated. In this review, we present findings that aid in understanding how vector-borne flavivirus persistence is established in wildlife. Research studies to be discussed include determining the critical roles universal flavivirus non-structural proteins played in flaviviral persistence, the advancement of animal models of viral persistence, and studying host factors that allow vector-borne flavivirus replication without destructive effects on infected cells. These findings underscore the viral–host relationships in wildlife animals and could be used to elucidate the underlying mechanisms responsible for the establishment of viral persistence in these animals.
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Gibbs, Tristan, and David J. Speers. "Neurological disease caused by flavivirus infections." Microbiology Australia 39, no. 2 (2018): 99. http://dx.doi.org/10.1071/ma18029.

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The Flavivirus genus contains dozens of species with varying geographical distributions. Most flavivirus infections in humans are asymptomatic or manifest as a non-specific febrile illness, sometimes accompanied by rash or arthralgia. Certain species are more commonly associated with neurological disease and may be termed neurotropic flaviviruses. Several flaviviruses endemic to Australia and our near northern neighbours are neurotropic, such as Murray Valley encephalitis virus, West Nile (Kunjin) virus and Japanese encephalitis virus. Flavivirus neurological disease ranges from self-limiting meningitis to fulminant encephalitis causing permanent debilitating neurological sequelae or death. The recent Zika virus outbreak in South America has highlighted the dramatic effects of flavivirus neurotropism on the developing brain. This article focuses on the neurotropic flaviviruses endemic to Australia and those of international significance.
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Dissertations / Theses on the topic "Flavivirus"

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Shomiad, Shueb Rafidah Hanim. "Contribution of different components of innate and adaptive immunity to severity of flavivirus-induced encephalitis in susceptible and resistant hosts." University of Western Australia. School of Biomedical, Biomolecular and Chemical Sciences, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0199.

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[Truncate abstract] Flaviviruses are small, positive-stranded RNA viruses belonging to the family Flaviviridae. Flavivirus infection in humans could cause diseases ranging from febrile illnesses to fatal encephalitis. Mice provide a useful small animal model to study flavivirus-induced encephalitis in humans since mice also develop encephalitis during flavivirus infection. Some strains of mice have been shown to be resistant to flavivirus challenge and this resistance is conferred by a single autosomal dominant gene, designated as Flvr. Recently, OAS1b gene has been identified to be a gene candidate for Flvr. Several congenic resistant mouse strains have been developed by introducing resistance genes from outbred or wild mice onto the genetic background of susceptible C3H mice. These new resistant strains that carry different allelic variants at the Flv locus include C3H/PRI-Flvr (RV), C3H.MOLD-Flvmr (MOLD) and C3H.M.domesticus-Flvr-like (DUB), the latter two being developed in the same laboratory in which the work described in this thesis was accomplished. Preliminary studies in this laboratory found that flavivirus resistant mice are vulnerable to certain flavivirus infections, particularly when challenged by intracerebral (i.c.) route. Intracerebral (i.c.) challenge with flaviviruses such as West Nile virus (WNV) Sarafend strain and Kunjin virus (KUNV) MRM16 strain were found to induce high mortality in flavivirus resistant mice while infection with Murray Valley encephalitis virus (MVEV) OR2 strain did not cause any apparent disease in the same mice. ... Thus, it can be concluded that CD8+ T cells exerted harmful effect to resistant DUB mice during KUNV i.c. infection by producing excessive IFN[gamma] that could be toxic, causing functional loss of the CNS cells. It was shown from in vitro studies that WNV had the highest tropism for macrophages and dendritic cells, followed by KUNV. MVEV however did not replicate well in these cells. This combined with the data from the in vivo studies indicates that macrophages might be involved in the pathogenesis of intraperitoneal (i.p.) infection of WNV but not KUNV and MVEV. The reason for this could be that the production of KUNV in macrophages may not be high enough to induce viraemia and subsequent fatal encephalitis in mice. In contrast, MVEV appears to use different mechanism or cells for virus dissemination. Although macrophages may not be involved in KUNV pathogenesis after i.p. infection, the fact that macrophages support KUNV replication in vitro may indicate the possibility that blood-borne macrophages were recruited to the brain where they can get infected with KUNV during i.c. infection and therefore could participate in KUNV pathogenesis in DUB mice. This study provides evidence for the first time on the detrimental effect of host antiviral immunity and inflammatory mediators during flavivirus i.c. infection in resistant mice. However, it also launches a new question on the selective cell tropism of KUNV versus MVEV responsible for inducing different pattern of immune responses and consequently leading to different outcomes of infection in resistant mice.
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Khou, Cécile. "Etude du neurotropisme des Flavivirus neuropathogènes." Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCC305/document.

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Les Flavivirus neuropathogènes, tels que le virus de l’encéphalite japonaise (JEV), le virus West Nile (WNV), le virus de la fièvre jaune (YFV) et le virus Zika (ZIKV) causent des maladies neurologiques. Ces maladies sont dues à une infection des cellules du système nerveux central (CNS) par ces virus. Le CNS est un organe privilégié, isolé des agents pathogènes par une barrière entre le sang et le cerveau, appelée barrière hémato-encéphalique (BBB). Les Flavivirus neuropathogènes capables de traverser cette BBB afin d’atteindre leurs cellules cibles, localisées dans le CNS, sont neuroinvasifs. Le but de cette étude est de comprendre les mécanismes cellulaires permettant aux Flavivirus de traverser la BBB et les effets de l’infection par les virus ZIKV et WNV des cellules du CNS sur le développement de celles-ci.Le YFV est un virus hépatotrope, infectant majoritairement le foie et les reins. Deux vaccins vivants atténués dirigés contre le YFV, le vaccin FNV (pour French Neurotropic Virus) et le vaccin 17D, ont été obtenus empiriquement par passages successifs de souches virulentes de YFV sur cerveaux de souriceaux. Ces vaccins ne causent plus de maladies touchant les reins et le foie, mais peuvent parfois causer des encéphalites post-vaccinales. Ces cas d’encéphalites démontrent que ces souches vaccinales sont devenues neurovirulentes mais aussi neuroinvasives car les virus ont pu franchir la BBB. A cause d’une incidence trop élevée d’encéphalites post-vaccinales par rapport au vaccin 17D, le vaccin FNV a été retiré du marché dans les années 1980.Le JEV est un virus neurotrope, causant des encéphalites graves en Asie du Sud-Est. A ce jour, il existe un vaccin vivant atténué, le JEV SA14-14-2, obtenu empiriquement par passages successifs d’une souche virulente sur cellules de hamster. Ce vaccin est moins neurovirulent et moins neuroinvasif que les souches virulentes de JEV en modèle de souris, et protège contre des infections humaines par le JEV. Cependant, des cas d’encéphalites ont été rapportés après injection de ce vaccin. Il apparait donc que, dans certains cas, la souche vaccinale JEV SA14-14-2 est capable de traverser la BBB et d’infecter les cellules neuronales. Les dernières épidémies à virus ZIKV en Polynésie Française et en Amérique du Sud ont induit une augmentation de cas de malformations congénitales dans les zones touchées. Cela a soulevé de nouvelles questions quant à la capacité d’un Flavivirus à provoquer des malformations congénitales du CNS. Dans cette étude, nous avons identifié les mécanismes cellulaires permettant aux Flavivirus de traverser la BBB et les effets de l’infection par les virus ZIKV et WNV des cellules du CNS sur le développement de celles-ci.Nous avons utilisé deux systèmes in vitro permettant d’étudier le développement du CNS et la neuroinvasion des Flavivirus. Un premier système consiste en l’infection de coupes de cerveaux d’embryon de souris. En utilisant ce système, nous avons montré que le ZIKV a un tropisme préférentiel pour les cellules progénitrices de neurones, alors que le WNV a un tropisme préférentiel pour les neurones. Nous avons également montré que l’infection des progéniteurs neuronaux par le ZIKV induit un arrêt de la mitose cellulaire, alors que l’infection par le WNV n’a aucun effet sur la mitose. L’étude sur l’effet apoptotique de l’infection par les deux virus WNV et ZIKV n’a montré aucune différence entre les deux virus à des temps précoces d’infection.Un deuxième système a été mis au point pour l’étude de la neuroinvasion par les Flavivirus neuropathogènes. Ce système est composé de cellules endothéliales hCMEC/D3 pouvant former des jonctions serrées. Ces cellules ont été cultivées sur filtres d’insert de puits de culture cellulaire Transwell, placés au-dessus de cellules neuronales humaines. A l’aide de ce système, nous avons comparé la capacité à traverser la BBB de plusieurs Flavivirus
Neuropathogenic Flaviviruses, such as Japanese encephalitis virus (JEV), West Nile virus (WNV), yellow fever virus (YFV) and Zika virus (ZIKV), cause neurological diseases. These diseases are due to viral infection of central nervous system (CNS) cells. The CNS is a privileged organ, isolated from pathogenic agents by a barrier between the blood and the barrier, called the blood-brain barrier (BBB). Neuropathogenic Flaviviruses which can cross this BBB in order to reach their target cells in the CNS, are neuroinvasive. This study aims at understanding the cellular mechanisms by which YFV and JEV Flaviviruses cross the BBB and the effects of viral infection by WNV and ZIKV of the CNS cells during neocortex development.YFV is a hepatrotopic virus, which mostly infects the liver and the kidneys. The two live-attenuated vaccines against YFV, the FNV (for French Neurotropic Virus) vaccine and the 17D vaccine, were obtained empirically by several passages in suckling mouse brain of YFV virulent strains. These vaccines do not cause any disease targeting the liver or the kidneys, but can sometimes cause post-vaccine encephalitis. These encephalitis cases suggest that the vaccine strains have become neurovirulent and neuroinvasive. Due to high risks of post-vaccine encephalitis, the FNV vaccine use was discontinued in the 1980s.JEV is a neurotropic virus, causing acute encephalitis in South East Asia. To date, there is a live-attenuated vaccine against JEV, the JEV SA14-14-2 vaccine, which was obtained empirically by several passages in primary hamster kidney cells. This vaccine is less neurovirulent and less neuroinvasive than JEV virulent strains in mouse model, and it protects against JEV infections. However, some cases of post-vaccine encephalitis were reported. It thus seems that, in some cases, the vaccine strain JEV SA14-14-2 is able to cross the BBB and infect neuronal cells.The recent ZIKV epidemics in French Polynesia and South America were linked to an increase in the number of congenital malformations, rising questions regarding the capacity of a Flavivirus to induce CNS congenital malformations.In this study, we have identified cellular mechanisms involved in Flavivirus neuroinvasion and studied the effect of ZIKV and WNV infection of neuronal cells under development.To study CNS development, we have infected mouse embryos brain slices. We were able to show that ZIKV has a preferential tropism for neuronal progenitors, whereas WNV has a preferential tropism for neuronal cells. We also show that infection of neuronal progenitors by ZIKV impairs the cell life cycle, whereas no effect on the cell life cycle was observed for WNV-infected cells. Studies on apoptosis induction did not show any difference between both viruses at early time points of infection.To study Flavivirus neuroinvasion, we have used an in vitro model of BBB composed of human endothelial hCMEC/D3 cells that can form tight junctions. These cells were cultivated on Transwell inserts and placed above human neuronal cells. Using this system, we show that YFV FNV cross the BBB more efficiently than YFV 17D, suggesting that YFV FNV is more neuroinvasive than YFV 17D. This observation can explain the higher post-vaccine encephalitis risks associated with YFV FNV vaccine compared to YFV 17D vaccine. We also confirmed that JEV SA14-14-2 vaccine strain is less neuroinvasive than JEV RP9.We also examined how JEV crosses the BBB and the endothelial cell response following JEV treatment. We show that both JEV RP9 and SA14-14-2 are able to cross the BBB without infecting its endothelial cells and without disrupting the BBB. Preliminary results suggest that JEV RP9, but not JEV SA14-14-2, crosses the BBB by dynamin-dependant transcytosis. Transcriptomic analysis of endothelial cells treated by either virus show slight, but significant, differences in regulation of genes implicated in several pathways associated with CNS diseases
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Lequime, Sébastian. "Interactions flavivirus-moustiques : diversité et transmission." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066081/document.

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Les flavivirus sont des virus à ARN parmi lesquels certains sont des arbovirus transmis entre hôtes vertébrés par des vecteurs arthropodes, notamment des moustiques. L'interaction avec les moustiques est centrale dans la biologie des flavivirus par son influence sur leur diversité génétique et transmission, mais certains de ses aspects restent méconnus. Au cœur de cette thèse, des approches basées sur les « big data », générées par des technologies modernes ou par compilation de travaux plus anciens, ont éclairé d’un jour nouveau la complexité des relations moustique-flavivirus. En explorant des génomes de moustiques anophèles, nous avons identifié et caractérisé des éléments viraux endogènes d'origine flavivirale chez Anopheles sinensis et An. minimus, suggérant l'existence de flavivirus infectant les anophèles et révélant une facette insoupçonnée de leur diversité. Par ailleurs, nous avons exploré, par séquençage haut-débit, la fine interaction entre le génotype du moustique Aedes aegypti et la diversité intra-hôte du virus de la dengue-1. Nos résultats montrent un fort effet de la dérive génétique lors de l'infection initiale, diminuant l'importance relative de la sélection naturelle, et une modulation de la diversité génétique intra-hôte du virus par le génotype du moustique. Enfin, nous avons compilé la littérature sur la transmission verticale des arbovirus chez les moustiques, c'est-à-dire de la femelle infectée à sa descendance, afin d'identifier des facteurs techniques et biologiques sous-jacents. Nos résultats améliorent la compréhension de ce mode de transmission et des stratégies employées par les arbovirus pour persister dans l’environnement
Flaviviruses are RNA virus among which some are arboviruses transmitted between vertebrate hosts and arthropod vectors, like mosquitoes. The interaction with mosquitoes is key in the biology of flaviviruses because it influences their genetic diversity and transmission. However, some aspects however are still poorly understood. At the heart of the work presented in this dissertation, strategies based on ‘big data’, both by taking advantage of modern technologies and by compiling older literature, highlighted new aspects of the complex relationships between flaviviruses and mosquitoes. While exploring Anopheles mosquito genomes, we identified and characterized endogenous viral elements of flaviviral origin in Anopheles sinensis and An. minimus, which supports the existence of flaviviruses infecting Anopheles mosquitoes and highlights new aspected of their diversity. Besides, we explored, by deep sequencing, the fine-tuned interaction between genotypes of the mosquito Aedes aegypti and the intra-host diversity of dengue virus 1. Our results showed a strong effect of genetic drift during initial infection, reducing the relative importance of natural selection, and a modulation of the intra-host viral genetic diversity by the mosquito genotype. Finally, we assembled the litterature on arbovirus vertical transmission in the mosquito vector, i.e. from an infected female to her offspring, in order to identify underlying technical and biological predictors. Our results increase our understanding of this transmission mode and the strategies employed by arboviruses to persist in their environment
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Lequime, Sébastian. "Interactions flavivirus-moustiques : diversité et transmission." Electronic Thesis or Diss., Paris 6, 2016. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2016PA066081.pdf.

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Les flavivirus sont des virus à ARN parmi lesquels certains sont des arbovirus transmis entre hôtes vertébrés par des vecteurs arthropodes, notamment des moustiques. L'interaction avec les moustiques est centrale dans la biologie des flavivirus par son influence sur leur diversité génétique et transmission, mais certains de ses aspects restent méconnus. Au cœur de cette thèse, des approches basées sur les « big data », générées par des technologies modernes ou par compilation de travaux plus anciens, ont éclairé d’un jour nouveau la complexité des relations moustique-flavivirus. En explorant des génomes de moustiques anophèles, nous avons identifié et caractérisé des éléments viraux endogènes d'origine flavivirale chez Anopheles sinensis et An. minimus, suggérant l'existence de flavivirus infectant les anophèles et révélant une facette insoupçonnée de leur diversité. Par ailleurs, nous avons exploré, par séquençage haut-débit, la fine interaction entre le génotype du moustique Aedes aegypti et la diversité intra-hôte du virus de la dengue-1. Nos résultats montrent un fort effet de la dérive génétique lors de l'infection initiale, diminuant l'importance relative de la sélection naturelle, et une modulation de la diversité génétique intra-hôte du virus par le génotype du moustique. Enfin, nous avons compilé la littérature sur la transmission verticale des arbovirus chez les moustiques, c'est-à-dire de la femelle infectée à sa descendance, afin d'identifier des facteurs techniques et biologiques sous-jacents. Nos résultats améliorent la compréhension de ce mode de transmission et des stratégies employées par les arbovirus pour persister dans l’environnement
Flaviviruses are RNA virus among which some are arboviruses transmitted between vertebrate hosts and arthropod vectors, like mosquitoes. The interaction with mosquitoes is key in the biology of flaviviruses because it influences their genetic diversity and transmission. However, some aspects however are still poorly understood. At the heart of the work presented in this dissertation, strategies based on ‘big data’, both by taking advantage of modern technologies and by compiling older literature, highlighted new aspects of the complex relationships between flaviviruses and mosquitoes. While exploring Anopheles mosquito genomes, we identified and characterized endogenous viral elements of flaviviral origin in Anopheles sinensis and An. minimus, which supports the existence of flaviviruses infecting Anopheles mosquitoes and highlights new aspected of their diversity. Besides, we explored, by deep sequencing, the fine-tuned interaction between genotypes of the mosquito Aedes aegypti and the intra-host diversity of dengue virus 1. Our results showed a strong effect of genetic drift during initial infection, reducing the relative importance of natural selection, and a modulation of the intra-host viral genetic diversity by the mosquito genotype. Finally, we assembled the litterature on arbovirus vertical transmission in the mosquito vector, i.e. from an infected female to her offspring, in order to identify underlying technical and biological predictors. Our results increase our understanding of this transmission mode and the strategies employed by arboviruses to persist in their environment
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Grard, Gilda. "Génomique et évolution des flavivirus transmis par les tiques et découverte d'un nouveau lignage du genre flavivirus." Aix-Marseille 2, 2006. http://www.theses.fr/2006AIX20679.

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Gollins, S. W. "Mechanisms of flavivirus neutralization and cellular infection." Thesis, University of Oxford, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.355752.

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Dayaraj, Cecilia. "Molecular and immunological studies on flavivirus virulence." Thesis, University of Oxford, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.279888.

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Carney, Jennifer. "Viral Determinants of Flavivirus Neurotropism in Humans." Thesis, University of Liverpool, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.526956.

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Pacca, Carolina Colombelli. "Screening de novos antivirais inibidores de flavivirus." Faculdade de Medicina de São José do Rio Preto, 2013. http://bdtd.famerp.br/handle/tede/201.

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Introduction. Arboviruses, arthropod-borne viruses, are frequently associated with human outbreaks and represent a serious health problem. The genus Flavivirus, which includes both the Yellow Fever Virus (YFV) and Saint Louis Encephalitis Virus (SLEV), are important pathogens that result in high morbidity and mortality rates worldwide. In Brazil, YFV has a sylvatic cycle and occurs annually, despite the efficiency of the vaccine. Saint Louis Encephalitis is an infectious illness that can cause acute fever caused by SLEV, which is widely distributed in the Americas. The emergence of SLEV became a serious concern after the first related outbreak in Brazil in 2006, in the city of Sao Jose do Rio Preto. There is no specific antiviral drug for these viruses, only supporting treatment that can alleviate the symptoms and prevent complications. The need to develop effective and safe antiviral drugs is indispensable for the treatment of these infections. Objective. The aim of this work was to identify new possible antiviral drugs against the arboviruses that can cause acute fever and encephalitis (YFV and SLEV) and to evaluate the capacity of inhibition of these compounds in ABR mice. Material and Methods. Plaque reduction assay, flow citometry, immunofluorescence and cellular viability were used to test the compounds in vitro. ABR mice were inoculated with YFV, and the biological samples were tested for the presence of the virus through the use of plaque reduction assay and qPCR. Neutralization assay was also performed. Results. Treated cells showed efficient inhibition of viral replication at concentrations that presented minimal toxicity to the cells. The assays showed that ftalyl-tiazole and fenoxytiosemicarbazone were more effective, and that they reduced viral replication by 60% and 75% for YFV and SLEV, respectively. The analysis also revealed that the ABR mice inoculated with YFV had histopathological alterations in the liver; however, the samples did not present viral title. Neutralization assay showed a high concentration of antibodies in the serum. Conclusion. The inhibitions of viral replication were confirmed through the use of some assays in vitro, and the effectiveness of the selected compounds show that they are an option in the treatment of these viruses. More detailed studies are needed to determine the mechanism of action of these molecules. The mice were found to have histopathological alterations, which indicates viral infection; however, they also presented with high concentrations of antibodies. More studies about animal models are necessary to make in vivo experiments.
Introdução: Os arbovírus, vírus transmitidos por artrópodes, são freqüentemente associadas a surtos em seres humanos e representam um problema sério de saúde pública. Os vírus pertencentes ao gênero Flavivirus, tais como vírus da Febre Amarela (YFV) e vírus da Encefalite de Saint Louis (SLEV), são importantes patógenos que podem causar alta taxa de morbidade e mortalidade no mundo. No Brasil, YFV é mantido em ciclo silvestre notificados anualmente, a despeito da segurança e eficiência da vacina. A encefalite de Saint Louis é uma doença infecciosa febril aguda causada pelo SLEV amplamente distribuída nas Américas. A emergência do SLEV passou a ser um fato preocupante no Brasil a partir da constatação do primeiro surto no país em 2006, na cidade de São Jose do Rio Preto. Não existe tratamento específico para estas viroses, somente tratamento de suporte para ajudar a aliviar os sintomas e prevenir complicações. Desta forma, há uma grande necessidade de que sejam desenvolvidos antivirais efetivos e seguros para o tratamento destas infecções. Objetivos: O objetivo deste trabalho foi identificar potenciais compostos antivirais contra os arbovírus causadores de doença febril aguda e encefalites (YFV e SLEV) in vitro e avaliar a capacidade de inibição da replicação viral dos compostos in vivo em camundongos ABR. Materiais e Métodos: Para tanto, foram realizados ensaios de redução de placas, citometria de fluxo, imunofluorescencia, bem como testes de viabilidade celular para as analises in vitro. Além disto, camundongos ABR foram inoculados com YFV e seus materiais biológicos testados para a presença de partículas virais por ensaio de redução de placas e qPCR. Adicionalmente, foi realizado ensaio de neutralização do soro dos animais. Resultados: Celulas tratadas com os compostos mostraram eficiente inibição da replicação viral em concentrações que apresentam baixa citotoxicidade. Os ensaios mostraram que derivados de ftalyl-tiazole e fenoxytiosemicarbazone foram os mais eficazes na ação antiviral, apresentando redução de 60% e 75% para YFV e SLEV, respectivamente. Camundongos ABR inoculados com YFV apresentaram alterações histológicas no fígado, entretanto, não foi constatado título viral nas amostras testadas. O ensaio de neutralização mostra altas concentrações de anticorpos no soro dos animais. Conclusões: A inibição da replicação foi comprovada por vários ensaios in vitro evidenciando as moléculas como potentes alternativas para o tratamento dos vírus. Mais estudos são necessários para a determinação do mecanismo de ação destas moléculas. Os camundongos apresentaram alterações histopatológicas sendo um indicativo de infecção, entretanto, apresentam altas taxas de anticorpos. Mais estudos sobre modelo animal são necessários para a realização de ensaios in vivo.
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Singethan, Katrin. "Untersuchungen zur Inhibition Paramyxo- und Flavivirus-induzierter Membranfusion." kostenfrei, 2009. http://www.opus-bayern.de/uni-wuerzburg/volltexte/2009/3634/.

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Books on the topic "Flavivirus"

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Gregory, Bock, Goode Jamie, Novartis Foundation, and Novartis Institute for Tropical Diseases., eds. New treatment strategies for dengue and other flaviviral diseases. Chichester: John Wiley & Sons, 2006.

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Shi, Pei-Yong. Molecular virology and control of flaviviruses. Norfolk, UK: Caister Academic Press, 2012.

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M, Chambers Thomas, ed. The flaviviruses. Oxford: Academic, 2004.

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M, Chambers Thomas, ed. The flaviviruses. Oxford: Academic, 2004.

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Chambers, Thomas J. The Flaviviruses: Detection, Diagnosis and Vaccine Development. Burlington: Elsevier, 2003.

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M, Chambers Thomas, Monath Aaron J, Maramorosch Karl, Murphy Frederick A, and Shatkin Aaron J, eds. Advances in virus research. Amsterdam: Elsevier, 2004.

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M, Chambers Thomas, Monath Aaron J, Maramorosch Karl, Murphy Frederick A, and Shatkin Aaron J, eds. Advances in virus research. Amsterdam: Oxford, 2003.

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Bock, Gregory, and Jamie Goode, eds. New Treatment Strategies for Dengue and Other Flaviviral Diseases. Chichester, UK: John Wiley & Sons, Ltd, 2006. http://dx.doi.org/10.1002/0470058005.

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Ruzek, Daniel, ed. Flavivirus Encephalitis. InTech, 2011. http://dx.doi.org/10.5772/847.

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Schlesinger, Milton J., and Sondra Schlesinger. Togaviridae and Flaviviridae. Springer, 2012.

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Book chapters on the topic "Flavivirus"

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Contigiani, Marta S., Luis A. Diaz, and Lorena Spinsanti. "Flavivirus." In Arthropod Borne Diseases, 73–88. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-13884-8_6.

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Harnett, Gerald B., and Julia A. Cattell. "Flavivirus." In PCR for Clinical Microbiology, 241–44. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9039-3_34.

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Gooch, Jan W. "Flavivirus." In Encyclopedic Dictionary of Polymers, 893. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13767.

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Westaway, Edwin G. "Flavivirus‡." In The Springer Index of Viruses, 461–71. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-95919-1_67.

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Reid, Hugh W., Herbert Weissenböck, and Károly Erdélyi. "Flavivirus Infections." In Infectious Diseases of Wild Mammals and Birds in Europe, 128–45. Oxford, UK: Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781118342442.ch9.

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Yu, Yufeng, Lulu Si, and Yu Meng. "Flavivirus Entry Inhibitors." In Advances in Experimental Medicine and Biology, 171–97. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-8702-0_11.

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Rice, Charles M., Ellen G. Strauss, and James H. Strauss. "Structure of the Flavivirus Genome." In The Togaviridae and Flaviviridae, 279–326. Boston, MA: Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4757-0785-4_10.

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Colombarolli, Stella Garcia, Izabella Cristina Andrade Batista, Naiara Clemente Tavares, Eneida Santos de Oliveira, Camila Sales Nascimento, Philip Louis Felgner, Rafael Ramiro de Assis, and Carlos Eduardo Calzavara-Silva. "Peptide Microarrays for Flavivirus Diagnosis." In Methods in Molecular Biology, 199–208. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2732-7_14.

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Padmanabhan, R., N. Mueller, E. Reichert, C. Yon, T. Teramoto, Y. Kono, R. Takhampunya, et al. "Multiple Enzyme Activities of Flavivirus Proteins." In Novartis Foundation Symposia, 74–86. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470058005.ch6.

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Kümmerer, Beate M. "Establishment and Application of Flavivirus Replicons." In Advances in Experimental Medicine and Biology, 165–73. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-8727-1_12.

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Conference papers on the topic "Flavivirus"

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Silva, Stephanie, Barbara Santos, Mariana Gomes, Ygara Mendes, Renata Pereira, Tiago Santos, Samir Campos, Vanessa Santos, Noemi Gardinali, and Sheila Lima. "Interference of EDTA on Flavivirus infectivity." In International Symposium on Immunobiologicals. Instituto de Tecnologia em Imunobiológicos, 2023. http://dx.doi.org/10.35259/isi.2023_58027.

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Chaley, M. B., Zh S. Tyulko, and V. A. Kutyrkin. "Specifics of Coding Sequences in the Flavivirus Genomes." In Mathematical Biology and Bioinformatics. Pushchino: IMPB RAS - Branch of KIAM RAS, 2018. http://dx.doi.org/10.17537/icmbb18.10.

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"Recognition of flavivirus species on the base of coding genome sequences." In Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-091.

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Chaley, M. B., Zh S. Tyulko, and V. A. Kutyrkin. "Fast Method to Recognize Flavivirus Species after Sequencing the Viral Genome." In Mathematical Biology and Bioinformatics. Pushchino: IMPB RAS - Branch of KIAM RAS, 2020. http://dx.doi.org/10.17537/icmbb20.12.

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woo Kim, Chan, Se Hwan Ahn, and Taeseon Yoon. "Comparison of flavivirus using datamining-Apriori, K-means, and decision tree algorithm." In 2017 19th International Conference on Advanced Communication Technology (ICACT). IEEE, 2017. http://dx.doi.org/10.23919/icact.2017.7890130.

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Santos, Franciellen Machado dos, VIVIANE HORN DE MELO, AMANDA PELLENZ RUIVO, FERNANDA M. S. GODINHO, and RICHARD STEINER SALVATO. "DETECÇÃO MOLECULAR DE ALPHAVIRUS E FLAVIVIRUS EM PACIENTES DO RIO GRANDE DO SUL." In IV Congresso Nacional de Microbiologia Clínica On-line. Revista Multidisciplinar em Saúde, 2024. http://dx.doi.org/10.51161/conamic2024/30268.

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Martins, Raquel, Carolina Cajaraville, Fernando Conte, and Márcia Arissawa. "Optimized production of monoclonal antibody used in Flavivirus immunoassays for different projects of vaccine development." In II Seminário Anual Científico e Tecnológico em Imunobiológicos. Instituto de Tecnologia em Imunobiológicos, 2014. http://dx.doi.org/10.35259/isi.sact.2014_28652.

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Lima, Michelle, Paloma Pêgo, Gabriel Silva, and Salvatore De Simone. "Identification of targeted epitopes of yellow fever virus based on homology with other species of flavivirus." In V Seminário Anual Científico e Tecnológico. Instituto de Tecnologia em Imunobiológicos, 2017. http://dx.doi.org/10.35259/isi.sact.2017_26145.

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Radzol, A. R. M., Khuan Y. Lee, W. Mansor, and I. S. Omar. "PCA criterion for SVM (MLP) classifier for flavivirus biomarker from salivary SERS spectra at febrile stage." In 2016 38th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2016. http://dx.doi.org/10.1109/embc.2016.7592146.

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Nandy, Ashesh, Sumanta Dey, Proyasha Roy, Subhas Basak, and Sukhen Das. "Comparison of Base Distributions in Dengue, Zika and Other Flavivirus Envelope and NS5 Genes." In MOL2NET 2017, International Conference on Multidisciplinary Sciences, 3rd edition. Basel, Switzerland: MDPI, 2017. http://dx.doi.org/10.3390/mol2net-03-04966.

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Reports on the topic "Flavivirus"

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Paul, Satashree. Flavivirus and its Threat. Science Repository, March 2021. http://dx.doi.org/10.31487/sr.blog.30.

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A number of studies found that the virus can activate the endothelial cells and affect the structure and function of the blood?brain barrier, promoting immune cell migration to benefit the virus nervous system target cells infected by flaviviruses.
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Fournier, Maurille J., and Thomas L. Mason. Structure and Expression of Genes for Flavivirus Immunogens. Fort Belvoir, VA: Defense Technical Information Center, January 1992. http://dx.doi.org/10.21236/ada252662.

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