Rozprawy doktorskie na temat „Encephalitis”
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Lewthwaite, Penelope. "Acute encephalitis, Japanese encephalitis, diagnostics and disability in Southeat Asia". Thesis, University of Liverpool, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.548757.
Pełny tekst źródłaThomson, Alan J. G. "Multifocal cysticercal encephalitis". Thesis, University of Cape Town, 1991. http://hdl.handle.net/11427/25955.
Pełny tekst źródłaSissons, James Robert. "Pathogenesis of Alanthamoeba encephalitis". Thesis, Birkbeck (University of London), 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.429097.
Pełny tekst źródłaMatin, Abdul. "Pathogenesis of Balamuthia amoebic encephalitis". Thesis, Birkbeck (University of London), 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.500082.
Pełny tekst źródłaIrani, Sarosh R. "Antibody targets in autoimmune encephalitis". Thesis, University of Oxford, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.533850.
Pełny tekst źródłaWinter, Peter Mark. "The human response to Japanese encephalitis". Thesis, University of Liverpool, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398577.
Pełny tekst źródłaNicolle, Della. "The impact of anti-NMDAR encephalitis". Thesis, Cardiff University, 2017. http://orca.cf.ac.uk/104235/.
Pełny tekst źródłaGranerod, Julia. "Encephalitis in England : incidence and cause". Thesis, London School of Hygiene and Tropical Medicine (University of London), 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.549752.
Pełny tekst źródłaBera, Katarzyna D. "Autoantibodies to N-methyl D-aspartate receptors in autoimmune encephalitis". Thesis, University of Oxford, 2011. http://ora.ox.ac.uk/objects/uuid:6bbda982-ab5c-4982-b23a-0478c689869c.
Pełny tekst źródłaPetit, Pedrol Mar. "Antigens and mechanisms of immune-mediated encephalitis". Doctoral thesis, Universitat de Barcelona, 2018. http://hdl.handle.net/10803/664343.
Pełny tekst źródłaINTRODUCCIÓN: La encefalitis autoimmune representa una nueva categoria de enfermedades immunomediadas del cerebro que estan mediadas por anticuerpos dirigidos contra receptores sinápticos, canales iónicos o proteinas neuronales de superfície. De entre todas las encefalitis consideradas idiopaticas, hay un subgrupo, probablemente immunomedidos, pendientes de ser identificadas. En los ultimos 11 años, 16 subtipos de encefalitis idiopaticas han sido identificadas como immunomediadas. La identificación de estas enfermedades es importante porque, aunque son potencialmente letales, son curables si se identifican rapid de nuevas en amente y se tratan. El estudio de estas enfermedades ha permitido el descubrimiento de nuevos mecanismos de alteración de la sinapsi medidados por anticuerpos que dan lugar a alteraciones de comportamiento y de memoria, epilepsia, movimientos anormales, o bajo nivel de consciencia. OBJETIVOS: 1) Identificar pacientes con encefalitis de etiologia desconocida, pero con caracteristicas clinicas y paraclinicas que sugieren una causa immunomedidada; 2) Caracterizar nuevos autoanticuerpos asociados a estos trastornos asi como las dianas antigenicas, y desarrollar pruebas diagnosticas inequivocas, y 3) determinar en modelos animales como los autoanticuerpos alteran el nivel y funcion de de los antigenos neuronales sinápticos (NMDAR y LGI1). MÉTODOS: Se usaron secciones de cerebro de rata y cultivos primarios de neuronas hipocampales de rata para la identificación de nuevos anticuerpos contra proteinas neuronales en muestras de suero y liquido cefaloraquideo (LCR) de pacientes. Para la detección de los anticuerpos se usó immunohistoquimica, immunocitoquimica de neuronas y en células HEK293 transfectadas. El aislamiento de nuevos antigeno diana se hizo mediante la immunoprecipitacion de proteinas de superficie neuronal con anticuerpos de los pacientes, y posterior caracterización por espectometria de masas. Para determinar el efecto patogenico de los anticuerpos de los pacientes, durante 14 dias los ratones fueron expuestos de manera cerebroventricular a los anticuerpos mediante la implantación subcutanea de bombas osmoticas, y posteriormente se analizó el efecto sobre las dianas antigenicas asi como alteraciones de comportamiento y memoria. Para ello, se usaron tecnicas de microscopia confocal cuantitativa de los niveles de antigenos sinápticos, immunoprecipitación de los anticuerpos unidos al tejido cerebral, immunoblot de las proteinas precipitadas, electrofisiologia en secciones de cerebro de raton, y una bateria de pruebas de comportamiento estandarizadas. Todos los estudios se realizaron en dias determinados de exposición a los anticuerpos (fase de la enfermedad), asi como después de la infusión (fase de recuperación). RESULTADOS: (1) Se identificaron dos nuevas encefalitis autoimmunes: encefalitis anti-GABAaR y encefalitis anti-neurexin-3α. La encefalitis anti-GABAaR puede afectar niños y adultos, esta asociada con crisis epilepticas y anormalidades en la resonancia magnetica del cerebro, y es tratable con immunoterapia. En algunos pacientes la respuesta immune se desencadena por la presencia de un tumor. La encefalitis anti-neurexin-3α manifiesta con un sindrome menos distintivo, a menudo se asocia con crisis epilepticas y tambien es tratable con immunoterapia. No se ha identificado asociacion tumoral. (2) La diana antigenica de los anticuerpos de la encefalitis anti-GABAaR se encuentra principalmente en las subunidades alfa1 y β3, y menos frecuentemente en la subunidad γ2. Mientras que las subunidades alfa1 y β3 son relevantes para la enfermedad, la presencia de anticuerpos adicionales contra γ2 no modifica el fenotipo de la enfermedad. Los anticuerpos anti-GABAaR producen una disminución de los niveles de GABAaR totales y sinapticos, apoyando su patogenicidad. (3) La immunoprecipitación de la diana antigenica de pacientes con encefalitis anti-neurexin-3α demostró que los epitopos estan localizados en la subunidad 3alfa, y no en su ligando postsinaptico LRRTM2. Estos autoanticuerpos causan una reducción del numero total de sinapsis asi como de la proteina presinaptica Bassoon, y de la postsinaptica Homer1, apoyando su patogenicidad. (4) La expresion recombinante de las subunidades antigenicas en celulas HEK293, pueden ser usadas como prueba diagnostica para identificar pacientes con estas encefalitis autoimmunes. (5) La infusión de anticuerpos NMDAR en el sistema cerebroventricular de ratones causa problemas de memoria, anhedonia, y comportamientos depresivos. Los anticuerpos infusionados se unen especificamente a los receptores NMDA del cerebro y provocan la disminución de la densidad de dichos receptores a nivel sinaptico y extrasinaptico. Estos efectos son reversibles despues de la suspension de la infusion de anticuerpos. (6) La administracion de ephrin-B2 antagoniza el efecto patogenico de los anticuerpos contra NMDAR de los pacientes, incluyendo los efectos de memoria, depresion, densidad de receptores NMDA y EphB2, y plasticidad sinaptica a largo plazo, pudiendo ser usado como estrategia terapeutica. (7) Los anticuerpos de los pacientes con encefalitis anti-LGI1 impiden la unión entre la proteina neuronal secretada LGI1 y la proteina presinaptica ADAM23 y la postsinaptica ADAM22. (8) La infusión de anticuerpos de los pacientes contra LGI1 en el sistema cerebroventricular de los ratones causa problemas de memoria, asi como disminución de los niveles de canales de potasio Kv1.1 presinapticos y de receptores AMPA postsinapticos. Estos efectos se asocian a una alteración de la plasticidad sinaptica e incremento de excitabilidad neuronal, de manera similar a los modelos de depleción genetica de LGI1. CONCLUSIONES: (1) Las encefalitis Anti-GABAaR y anti-neurexin-3α encephalitis son dos nuevas formas de encefalitis mediadas por anticuerpos. Hay evidencia que sostiene que estos anticuerpos son patogenicos, apoyando el concepto de que hay encefalitis sin caracterizar dentro de las muchas formas de encefalitis de causa desconocida. (2) La precipitación del antigeno neuronal es una estrategia excelente para aislar y caracterizar antigenos relevantes para la enfermedad, y poder desarrollar pruebas de detección. (3) Estos estudios han contribuido a desarrollar dos modelos animales de infusión de anticuerpos de encefalitis autoimmunes (NMDAR, LGI1) y a descubrir los cambios subyacentes mediados por anticuerpos en la función sináptica y la plasticidad. Los dos modelos cumplen con los criterios de Witebsky para enfermedades immunomediadas, y proporcionan la base para modelar otros trastornos neurológicos mediados por anticuerpos.
AÌlvarez, MariÌa C. Armesto. "Molecular studies of tick-borne encephalitis virus". Thesis, University of Oxford, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.413476.
Pełny tekst źródłaWatson, Robert J. "The role of autoantibodies in Rasmussen's encephalitis". Thesis, University of Oxford, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.409266.
Pełny tekst źródłaVander, Kelen Patrick. "Eco-Epidemiology of Eastern Equine Encephalitis Virus". Scholar Commons, 2013. http://scholarcommons.usf.edu/etd/4600.
Pełny tekst źródłaLo, Lily Yen-Ching. "Studies of Spanish influenza and encephalitis lethargica". Thesis, Queen Mary, University of London, 2003. http://qmro.qmul.ac.uk/xmlui/handle/123456789/1813.
Pełny tekst źródłaMichael, Benedict. "Detection and diagnosis of acute viral encephalitis". Thesis, University of Liverpool, 2014. http://livrepository.liverpool.ac.uk/2003409/.
Pełny tekst źródłaMohammad, Shekeeb S. "Early diagnosis of autoimmune encephalitis in children". Thesis, The University of Sydney, 2017. http://hdl.handle.net/2123/17298.
Pełny tekst źródłaWilliams, David Thomas. "Immunological and molecular studies on Japanese encephalitis virus with reference to the Australasuan region /". [St. Lucia, Qld.], 2001. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16236.pdf.
Pełny tekst źródłaAshok, M. S. "Evaluation Of The Efficacy Of DNA Vaccines For Japanese Encephalitis In A Murine Intracerebral Japanese Encephalitis Virus Challenge Model". Thesis, Indian Institute of Science, 2000. https://etd.iisc.ac.in/handle/2005/169.
Pełny tekst źródłaAshok, M. S. "Evaluation Of The Efficacy Of DNA Vaccines For Japanese Encephalitis In A Murine Intracerebral Japanese Encephalitis Virus Challenge Model". Thesis, Indian Institute of Science, 2000. http://hdl.handle.net/2005/169.
Pełny tekst źródłaGolovljova, Irina. "Viral zoonoses in Estonia : hantaviruses and tick-borne encephalitis virus : identification, prevalence, serological and genetic relationships /". Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-664-6/.
Pełny tekst źródłaOtter, Arthur. "A study of the neuropathogenesis of listerial encephalitis". Thesis, University of Cambridge, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.359880.
Pełny tekst źródłaMohammed, Manal Ahmed Farid. "Studies on zoonotic Japanese encephalitis virus Muar strain". Thesis, University of Liverpool, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.569545.
Pełny tekst źródłaTangkanond, Wipa. "Molecular Evolution of Japanese Encephalitis Virus in Nature". Thesis, University of Liverpool, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.526948.
Pełny tekst źródłaHenderson, A. "The epidemiology of Japanese encephalitis in Southern Nepal". Thesis, University of Nottingham, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.381421.
Pełny tekst źródłaVasconcelos, Daphne Y. "The cellular stress response in Measles Virus Encephalitis /". The Ohio State University, 2000. http://rave.ohiolink.edu/etdc/view?acc_num=osu1488194825668105.
Pełny tekst źródłaAva, Jessika Lane, i Jessika Lane Ava. "Spatiotemporal Analysis of Eastern Equine Encephalitis Human Incidence". Thesis, The University of Arizona, 2017. http://hdl.handle.net/10150/624117.
Pełny tekst źródłaBill, Sara. "Sanierung der Caprinen Arthritis-Encephalitis im Kanton Nidwalden /". [S.l.] : [s.n.], 1993. http://www.stub.unibe.ch/html/haupt/datenbanken/diss/bestell.html.
Pełny tekst źródłaHaglund, Mats. "Tick-borne encephalitis : prognosis, immunization and virus strain characterization /". Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4453-9/.
Pełny tekst źródłaMailles, Alexandra. "Epidémiologie, optimisation du diagnostic et pronostic des encéphalites infectieuses en France". Thesis, Grenoble, 2012. http://www.theses.fr/2012GRENV001.
Pełny tekst źródłaAbstract Background Despite a better knowledge about pathophysiological mechanisms and the generalisation of molecular biological Tools, the aetiology of encephalitis is still undetermined in most cases. Their incidence, the short-term and long-term prognosis of the disease and the persistence of sequelae are unknown. The objectives of this work were to improve the knowledge about the aetiology of encephalitis in France and to describe the patients hospitalized in France with encephalitis according to clinical, biological, demographic, epidemiological and outcome data. Methods Patients aged 28 days or more, who fitted the case definition, were enrolled in 2007. The investigation of aetiological diagnosis was carried out according to a previously defined diagnosis strategy. Epidemiological, clinical and biological data were collected using standardised questionnaires on admission, on day 5 of hospitalisation and on discharge. The study was carried out in accordance with French regulations. The long-term outcome of patients was assessed in 2010. Data collected encompassed persisting symptoms, resuming leisure activities, return to wok or resuming education and quality of life. Cognitive decline was assessed with patients' relatives using IQCODE. The main outcome measure was the Glasgow outcome scale (GOS). Results 253 patients presenting with acute encephalitis were included. A causative agent was identified for 131 (52%) of them. Most frequent causative agents were Herpes simplex virus (HSV, n=55), Varicella Zoster virus (VZV, n=20), Mycobacterium tuberculosis (n=20) and Listeria monocytogenes (n=13). Twenty-six patients (10%), died during hospitalisation. In 2010, 176 patients could be included and assessed. The outcome of encephalitis was favourable for 61% of patients and 39% had a poor outcome. Among patient employed before onset of encephalitis, 24% had not returned to work at the time of evaluation. Patients who presented with herpes encephalitis in 2007 had a lower score on GOS than other patients. Discussion Our study resulted in a important improvement of the proportion of encephalitis with a causative agent identified. We demonstrated that bacteria play a significant role as causes of encephalitis, and are responsible for most death occurring during the acute stage of encephalitis. An important proportion of patients presented long-term sequelae, illustrating the evolution of encephalitis from an acute infectious disease toward a chronic neurological disease. The high frequency of sequelae following herpes encephalitis is a shadow on the success of aciclovir. Conclusion Considering our results, we can propose recommendation for the everyday management of encephalitis patients, both to achieve aetiological diagnosis and a long-term follow-up that should be extended to all encephalitis patients. Herpes encephalitis should be more studied on pathophysiological aspects to explicate the severity of the disease despite the existence of a specific treatment, and to propose better prevention and management of sequelae
Хоменко, О. І. "Інтенсивна терапія гострих вірусних енцефалитів у дітей". Thesis, Видавництво СумДУ, 2008. http://essuir.sumdu.edu.ua/handle/123456789/14370.
Pełny tekst źródłaКоленко, Фаіна Григорівна, Фаина Григорьевна Коленко, Faina Hryhorivna Kolenko i Л. Е. Бражник. "Атипичное течение вирусных энцефалитов". Thesis, Видавництво СумДУ, 2004. http://essuir.sumdu.edu.ua/handle/123456789/9327.
Pełny tekst źródłaШолохова, Світлана Євгенівна, Светлана Евгеньевна Шолохова, Svitlana Yevhenivna Sholokhova, В. М. Псаррьов i П. І. Жук. "Кліщовий вірусний енцефаліт: епідеміологія, профілактика". Thesis, Видавництво СумДУ, 2008. http://essuir.sumdu.edu.ua/handle/123456789/14356.
Pełny tekst źródłaСміян, Олександр Іванович, Александр Иванович Смиян, Oleksandr Ivanovych Smiian, Тетяна Парфеніївна Бинда, Татьяна Парфеньевна Бында, Tetiana Parfeniivna Bynda i О. І. Хоменко. "Досвід використання цимевену у хворих на цитомегаловірусний енцефаліт". Thesis, Вид-во СумДУ, 2005. http://essuir.sumdu.edu.ua/handle/123456789/6685.
Pełny tekst źródłaJohansen, Cheryl Anne. "Investigation into the emergence of Japanese encephalitis virus in Australia /". St. Lucia, Qld, 2002. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16409.pdf.
Pełny tekst źródłaBorgo, Francesca. "When panthers are really pink and diamonds are black. Living things and "mass" kinds knowledge in Herpes Simplex Virus Encephalitis: new evidence for a theoretical redefinition of category specific effects". Doctoral thesis, SISSA, 2001. http://hdl.handle.net/20.500.11767/4648.
Pełny tekst źródłaLindblom, Pontus. "Epidemiological and Ecological Studies of Tick-borne Encephalitis Virus". Doctoral thesis, Linköpings universitet, Avdelningen för mikrobiologi och molekylär medicin, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-105921.
Pełny tekst źródłaBreakwell, Lucy. "The role of interferon in Semliki Forest virus encephalitis". Thesis, University of Edinburgh, 2006. http://hdl.handle.net/1842/29993.
Pełny tekst źródłaMelik, Wessam. "Molecular characterization of the Tick-borne encephalitis virus : Environments and replication". Doctoral thesis, Stockholms universitet, Institutionen för genetik, mikrobiologi och toxikologi, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-66950.
Pełny tekst źródłaAt the time of the doctoral defense, the following paper was unpublished and had a status as follows: Paper 4: Manuscript.
Shin, Hyunjin. "Characterization of monocyte subsets through the course of AIDS pathogenesis and correlations with the development of SIV-Encephalitis". Thesis, Boston College, 2010. http://hdl.handle.net/2345/2221.
Pełny tekst źródłaIndividuals infected with Human Immunodeficiency Virus (HIV) are susceptible to pathological abnormalities due to the infiltration of virus into different anatomical compartments. Monocytes are a heterogeneous population that undergoes changes in phenotype with HIV infection. It is hypothesized that changes in monocyte subsets observed through the course of infection will correlate with the development of SIV-Encephalitis (SIVE). 14 CD8+ T cell depleted rhesus macaques were infected with SIVmac251 and changes in 3 monocyte subsets, defined by their CD14 and CD16 surface expression as CD14+CD16-, CD14+CD16+, and CD14-CD16+, were tracked through the course of disease. The CD14+CD16- subset increased in the absolute number of cells and decreased in percentage of the total monocyte population. The CD14+CD16+ and CD14-CD16+ subsets increased in both absolute number and percentage. These changes have a biphasic dynamic that occurs during early infection and is pronounced in encephalitic animals. Several markers showed differential expression with infection and between subsets. Mac387, an early monocyte-macrophage marker, demonstrated a considerable decrease in expression. Concomitant with this change, CD68, CD163, CD44v6, CCR2, and CD64 increased expression in the total monocyte population, with the magnitude of these changes occurring in a subset-specific manner. In conclusion, monocyte subsets undergo changes with SIV infection that correspond to the development of encephalitis, highlighting the contribution of monocytes in neuroAIDS
Thesis (MS) — Boston College, 2010
Submitted to: Boston College. Graduate School of Arts and Sciences
Discipline: Biology
Van, den Hurk Andrew Francis. "The role of mosquitoes in the emergence of Japanese encephalitis virus in Australia /". St. Lucia, Qld, 2002. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16441.pdf.
Pełny tekst źródłaCavallaro, Kathleen F. "Evaluation of Surveillance for Acute (Meningitis) Encephalitis Syndrome (AES/AMES)". Digital Archive @ GSU, 2009. http://digitalarchive.gsu.edu/iph_theses/63.
Pełny tekst źródłaMyint, Khin Saw. "Neuropathogenesis of Japanese encephalitis in a rhesus monkey challenge model". Thesis, University of Liverpool, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.569249.
Pełny tekst źródłaPajek, Daniela. "Identifying chemokine receptors as plausible therapeutic targets in viral encephalitis". Thesis, University of Glasgow, 2013. http://theses.gla.ac.uk/4764/.
Pełny tekst źródłaHughson, M. D. "Micro-scale vaccine bioprocessing of a Japanese Encephalitis Virus vaccine". Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1427445/.
Pełny tekst źródłaAsghar, Naveed. "Ticks and Tick-borne Encephalitis Virus : From Nature to Infection". Doctoral thesis, Södertörns högskola, Miljövetenskap, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:sh:diva-31153.
Pełny tekst źródłaVektorburna sjukdomar är ett växande globalt hot mot både människor och djur. De pågående klimatförändringarna kan leda till förhöjda risker för infektioner överförda av myggor, fästingar och andra leddjursvektorer. Ixodes ricinus är en vanlig fästing i Europa som överför fästingburna patogener som är farliga för människor. Fästingburen encefalit (TBE) är en vektorburen sjukdom som orsakas av TBE-virus (TBEV). De pågående klimatförändringarna har bidragit till en ökning både av vektorn och sjukdomsfrekvensen. Mellan 10 000 och 15 000 mänskliga TBE-fall rapporteras årligen i Europa och Asien. Den geografiska fördelningen av TBEV visar ett ojämnt fördelningsmönster där viruset är koncentrerat till vissa fokusområden. TBEV återfinns i naturen i en livscykel där viruset hela tiden överförs mellan fästingar och däggdjur. Spridningen sker dels från en infekterad fästing till ett ryggradsdjur när fästingen äter på värddjuret. Spridning mellan fästingar sker troligen främst genom så kallad “co-feeding”, det vill säga att flera fästingar suger blod samtidigt från samma värddjur. Viruset kan då passera från en infekterad fästing, genom värddjuret till oinfekterade fästingar. Virus kan identifieras och studeras med genetiska metoder. Det ökande antalet TBE-fall i Skandinavien styrker vikten av att hitta och karakterisera ytterligare TBEV-stammar och identifiera nya naturliga fokusområden. Vi har sekvenserat och fylogenetiskt beskrivit fyra TBEV-stammar: Saringe-2009 (blodfylld nymf), JP-296 (födosökande vuxen hane), JP-554 (födosökande vuxen hane) och Mandal-2009 (födosökande nymfer, n = 10). Mandal-2009 är ett TBEV från ett naturligt fokusområde i södra Norge. Saringe-2009 kommer från ett naturligt fokusområde i norra Stockholms län, Sverige. JP-296 och JP-554 härstammar från Torö som är ett naturligt fokusområde i södra Stockholms län, Sverige. Förutom den genetiska sekvenseringen av TBEV har vi också studerat effekten av olika biotiska och abiotiska faktorer på populationsdynamik av I. ricinus i södra Stockholm och observerade variation i fästingsaktivitetsmönster både temporalt och spatialt. Förekomstmönster av fästinglarver, nymfer och vuxna honor, och det totala antalet fästingar är viktiga faktorer för sannolikheten för horisontell överföring av TBEV mellan fästingar. Vi fann att sannolikheten för synkron förekomst av larver, nymfer och honor var högst under försommaren. Vegetationshöjd, mängden skog och mängd öppet vatten runt undersökningsområden hade signifikanta negativa effekter på sannolikheten för att larver, nymfer och honor skulle förekomma samtidigt. Den variabla delen av den icke-kodande 3 ́regionen (3'NCR) av TBEV-genomet innehåller ofta en intern poly(A)-sekvens. Liksom andra RNA-virus, förekommer TBEV som så kallade ”quasispecies” vilka definieras som grupper av olika genetiska varianter av virus. Genom analysen av TBEV-stam Saringe-2009 avslöjades variation i poly(A)-sekvensen vilket indikerar förekomst av ”quasispecies”. Eftersom Saringe-2009 kom från en blodfylld nymf som hade sugit blod i > 60 timmar, föreslår vi att Saringe-2009 visar en förändring i ”quasispecies”-poolen när viruset överförs från exoterm fästingmiljö till endoterm däggdjursmiljö. Vi undersökte poly(A)-ekvensens variabilitet och dess roll vid replikering och för virulens hos TBEV, genom att skapa två infektiösa kloner av Torö-2003 stammen; en med en kort/vild-typ (A)3C(A)6 poly(A)-sekkvens, och en med en lång (A)3C(A)38 poly(A)-sekvens. Den infektiösa klonen med lång poly(A)-sekvens replikerade sämre än vildtypklonen i cellkultur, men (A)3C(A)38 poly(A) var mer virulent i C57BL/6-möss än (A)3C(A)6 poly(A). Datasimulering av TBEV-genomets sekundär-RNA-struktur visade att de längre poly(A)-sekvenserna påverkar veckningen av en specifik sekundärstruktur (SL14) i början av 3 ́NCR. Djupsekvenseringsanalys av TBEV-gnomen avslöjade skillnader för specifika gener och ”quasispecies”-strukturen efter passering i cellkultur och/eller mushjärna. Dessa förändringar föreslås bidra till de observerade skillnaderna i virulens. Våra resultat indikerar att den långa poly(A)-sekvensen ger instabilitet i TBEV-genomet, vilket resulterar i ökad mångfald av ”quasispecies”-populationen som i sin tur kan bidra till TBEV-virulens. Fylogenetisk analys av Saringe-2009, JP-296, JP-554 och Mandal-2009 visade på ett nära släktskap mellan de fyra skandinaviska TBEV-stammarna. De nya stammarna formerade ett kluster med en tidigare TBEV-stam identifierad på Torö (Toro-2003), vilket skapade ett skandinaviskt klad. Genetisk analys visade att Mandal-2009 innehåller en trunkerad 3 ́NCR som liknar den högvirulenta stammen HYPR. JP-296 och JP-554 hade däremot samma genetiska struktur som den längre Torö-2003 stammen från samma fokusområde. Djupsekvensering visade höge mångfald av ”quasispecies”-populationen för JP-296 och JP- 554 jämfört med Mandal-2009. Analys av enkel nukleotid polymorfism (SNP) visade att 40 % av alla SNP var gemensamma mellan ”quasispecies”-populationen för JP-296 och JP-554. Detta indikerar att TBEV-”quasispecies”-strukturen kan vara konserverad för närbesläktade virus vilken kan leda till att den bevaras inom specifika fokusområden. Sammantaget så visar dessa studier att miljöfaktorer påverkar förekomsten av fästingvektorn och dess olika livsstadier, vilket är en bakomliggande faktor för utbredning av TBEV i naturliga fokusområden. Det visar även på att värdmiljön påverkar strukturen för ”quasispecies”-populationen. Dessutom visar våra studier att evolution och utveckling av ”quasispecies”-strukturen kan påverka virulensen för TBEV i möss.
Rayamajhi, A. "Towards improving the management of acute encephalitis syndrome in Nepal". Thesis, University of Liverpool, 2016. http://livrepository.liverpool.ac.uk/3008419/.
Pełny tekst źródłaYu, Chao. "Pathogenesis induced by tick-borne encephalitis virus in epithelial cells". Doctoral thesis, Humboldt-Universität zu Berlin, Lebenswissenschaftliche Fakultät, 2014. http://dx.doi.org/10.18452/17046.
Pełny tekst źródłaTick-borne encephalitis virus (TBEV) is one of the most important vector-borne viruses in Europe and Asia. The transmission mainly occurs by the bite of an infected tick. Consuming of rough milk products from infected livestock animals also occasionally cause TBE cases. Human intestinal Caco-2 cells were used to investigate the pathogenesis caused by TBEV. During TBEV infection Caco-2 monolayers showed morphological changes with significant vacuolization. Ultrastructural analysis revealed dilatation of the rough endoplasmic reticulum and further enlargement to TBEV containing caverns. Caco-2 monolayers showed an intact epithelial barrier with stable transepithelial electrical resistance (TER). Concomitantly, viruses were detected in the basolateral medium, taken up via a transcytosis pathway. TBEV cell entry was efficiently blocked with different inhibitors, suggesting that actin filaments and microtubules are important for PI3K-dependent endocytosis. Moreover, experimental fluid uptake assay showed increased intracellular accumulation of FITC-dextran containing vesicles and co-localization of TBEV with early endosome antigen-1 and with sorting nexin-5 could confirm macropinocytosis as trafficking mechanism. In the late phase of infection, further evidence was found for translocation of virus via the paracellular pathway. Thus, TBEV pathomechanisms in human intestinal epithelial cells and its transmission via the alimentary route were enlightened. In addition, I investigated the effects of the two unfolded protein response (UPR) signaling pathways upon TBEV infection in Vero E6 cells. I showed that the amount of heat shock protein 72 increased in the course of TBEV infection. I then confirmed that TBEV infection activates the IRE1 pathway and ATF6 pathway. These findings provide the first evidence that TBEV infection activates the two UPR signaling pathways. Moreover, inhibition of UPR may provide a novel therapeutic strategy against TBE.
Passoni, Gabriella. "Unraveling viral encephalitis in vivo : dynamic imaging of neuro-invasion and neuro inflammation processes in the zebrafish". Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066644/document.
Pełny tekst źródłaThe zebrafish (Danio rerio) is an important model organism, particularly for studies of development and more recently host pathogen interactions. As opposed to other vertebrate model organisms, its optical clarity and ease of genetic manipulations allow to visualize highly dynamic cellular processes in vivo at the whole organism scale. These assets make the zebrafish a perfect model for the study of viral infections in vivo, such as those caused by neurotropic viruses. The aim of this project has been to gain insights in some of the interactions that determine encephalitis, by characterizing the neurotropic Sindbis virus (SINV). This Thesis project has consisted therefore in: 1) the development of a SINV infection model in zebrafish larvae, 2) the characterization of SINV neuroinvasion upon its inoculation in the bloodstream, thanks to the use of high resolution microscopy, 3) the study of SINV mechanism of entry in the CNS, 4) the characterization of the innate immune response, both at the whole organism and organ specific level. Thanks to the use of a SINV recombinant strain, engineered to express the green fluorescent protein “GFP” in infected cells upon viral replication, we have been able to follow the onset and the progression of the infection. We have suggested infection of peripheral neurons and subsequent axonal transport to the CNS as SINV entry mechanism. At the cellular level, we have identified neutrophils as the main IFN producing cells
da, Silva Oliveira Ana Rute. "Quantification of vector and host competence for Japanese Encephalitis Virus: a systematic review and meta-analyses of the literature". Thesis, Kansas State University, 2017. http://hdl.handle.net/2097/35518.
Pełny tekst źródłaDepartment of Diagnostic Medicine/Pathobiology
Natalia Cernicchiaro
Japanese encephalitis virus (JEV) is a virus of the Flavivirus genus that may result in encephalitis in vertebrate hosts. This vector-borne zoonosis occurs in Eastern and Southeastern Asia and an intentional or inadvertent introduction into the United States (US) would lead to important public health and economic consequences. The objective of this study was to gather, appraise, and synthesize primary research literature to identify and quantify vector and host competence for JEV, using a systematic review-metaanalysis (SR-MA) approach. After defining the research question, we performed a search in selected electronic databases. The title and abstract of the identified articles were screened for relevance using a defined set of exclusion and inclusion criteria, and relevant articles were subjected to a risk of bias assessment followed by data extraction. Random-effects subgroup meta-analysis models were fitted by species (mosquito or vertebrate host species) to estimate pooled summary measures as well as to compute the variance between studies. Meta-regression models were fitted to assess the association between different predictors and the outcomes of interest and to identify sources of heterogeneity among studies. Data were extracted from 171 peer-reviewed articles. Most studies were observational (59.06%) and reported vector competence (60.2%). The outcome measures reported pertained to transmission efficiency, host preference, and vector susceptibility to infection within vector competence; and susceptibility to infection within host competence. All outcome measures (JEV proportion of infection in vectors and hosts from observational studies; and JEV infection, dissemination, and transmission rates in vectors from experimental studies) had high heterogeneity. Mosquito species, diagnostic method, country, and capture method represented important sources of heterogeneity associated with the proportion of JEV infection in vectors; host species and region were considered sources of heterogeneity associated with the proportion of JEV infection in hosts; and diagnostic and mosquito capture methods were deemed important contributors of heterogeneity for the minimum infection rate (MIR) outcome. Mosquito species and administration route represented the main sources of heterogeneity associated with JEV infection rate in vectors. Quantitative estimates resulting from this SR-MA will be inputted into risk assessment models to evaluate risks associated with the introduction of JEV in the US.
Wright, Sukhvir. "Autoimmunity in idiopathic epilepsies and encephalopathies of childhood". Thesis, University of Oxford, 2014. https://ora.ox.ac.uk/objects/uuid:685944ee-8135-47ba-a90a-173fb195e3ec.
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