Relevant bibliographies by topics / Virus encephalitis

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Virus encephalitis'

Author: Grafiati
Published: 24 April 2022

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Journal articles on the topic "Virus encephalitis"

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Shindo, Atsuhiko, Genko Oyama, Noriko Nishikawa, and Nobutaka Hattori. "Varicella-zoster virus encephalitis resembling herpes simplex virus encephalitis." BMJ Case Reports 14, no. 12 (December 2021): e247602. http://dx.doi.org/10.1136/bcr-2021-247602.

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Vergara Centeno, J. L., L. González Zambrano, and J. M. Jáuregui Solórzano. "Zika virus encephalitis." Medicina Intensiva (English Edition) 43, no. 1 (January 2019): 59. http://dx.doi.org/10.1016/j.medine.2018.10.005.

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Chittick, Paul, John C. Williamson, and Christopher A. Ohl. "BK Virus Encephalitis." Annals of Pharmacotherapy 47, no. 9 (September 2013): 1229–33. http://dx.doi.org/10.1177/1060028013500646.

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Tan, Chong-Tin, and Kaw-Bing Chua. "Nipah virus encephalitis." Current Infectious Disease Reports 10, no. 4 (July 2008): 315–20. http://dx.doi.org/10.1007/s11908-008-0051-6.

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Jhan, Ming-Kai, Chia-Ling Chen, Ting-Jing Shen, Po-Chun Tseng, Yung-Ting Wang, Rahmat Dani Satria, Chia-Yi Yu, and Chiou-Feng Lin. "Polarization of Type 1 Macrophages Is Associated with the Severity of Viral Encephalitis Caused by Japanese Encephalitis Virus and Dengue Virus." Cells 10, no. 11 (November 15, 2021): 3181. http://dx.doi.org/10.3390/cells10113181.

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Infection with flaviviruses causes mild to severe diseases, including viral hemorrhagic fever, vascular shock syndrome, and viral encephalitis. Several animal models explore the pathogenesis of viral encephalitis, as shown by neuron destruction due to neurotoxicity after viral infection. While neuronal cells are injuries caused by inflammatory cytokine production following microglial/macrophage activation, the blockade of inflammatory cytokines can reduce neurotoxicity to improve the survival rate. This study investigated the involvement of macrophage phenotypes in facilitating CNS inflammation and neurotoxicity during flavivirus infection, including the Japanese encephalitis virus, dengue virus (DENV), and Zika virus. Mice infected with different flaviviruses presented encephalitis-like symptoms, including limbic seizure and paralysis. Histology indicated that brain lesions were identified in the hippocampus and surrounded by mononuclear cells. In those regions, both the infiltrated macrophages and resident microglia were significantly increased. RNA-seq analysis showed the gene profile shifting toward type 1 macrophage (M1) polarization, while M1 markers validated this phenomenon. Pharmacologically blocking C-C chemokine receptor 2 and tumor necrosis factor-α partly retarded DENV-induced M1 polarization. In summary, flavivirus infection, such as JEV and DENV, promoted type 1 macrophage polarization in the brain associated with encephalitic severity.
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Bondre, Vijay P., Gajanan N. Sapkal, Prasanna N. Yergolkar, Pradip V. Fulmali, Vasudha Sankararaman, Vijay M. Ayachit, Akhilesh C. Mishra, and Milind M. Gore. "Genetic characterization of Bagaza virus (BAGV) isolated in India and evidence of anti-BAGV antibodies in sera collected from encephalitis patients." Journal of General Virology 90, no. 11 (November 1, 2009): 2644–49. http://dx.doi.org/10.1099/vir.0.012336-0.

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During investigations into the outbreak of encephalitis in 1996 in the Kerala state in India, an arbovirus was isolated from a Culex tritaeniorhynchus mosquito pool. It was characterized as a Japanese encephalitis and West Nile virus cross-reactive arbovirus by complement fixation test. A plaque reduction–neutralization test was performed using hyperimmune sera raised against the plaque-purified arbovirus isolate. The sera did not show reactivity with Japanese encephalitis virus and were weakly reactive with West Nile virus. Complete open reading frame sequence analysis characterized the arbovirus as Bagaza virus (BAGV), with 94.80 % nucleotide identity with African BAGV strain DakAr B209. Sera collected from the encephalitic patients during the acute phase of illness showed 15 % (8/53) positivity for anti-BAGV neutralizing antibodies. This is the first report of the isolation of BAGV from India. The presence of anti-BAGV neutralizing antibodies suggests that the human population has been exposed to BAGV.
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Lobigs, Mario, Maximilian Larena, Mohammed Alsharifi, Eva Lee, and Megan Pavy. "Live Chimeric and Inactivated Japanese Encephalitis Virus Vaccines Differ in Their Cross-Protective Values against Murray Valley Encephalitis Virus." Journal of Virology 83, no. 6 (December 24, 2008): 2436–45. http://dx.doi.org/10.1128/jvi.02273-08.

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ABSTRACT The Japanese encephalitis virus (JEV) serocomplex, which also includes Murray Valley encephalitis virus (MVEV), is a group of antigenically closely related, mosquito-borne flaviviruses that are responsible for severe encephalitic disease in humans. While vaccines against the prominent members of this serocomplex are available or under development, it is unlikely that they will be produced specifically against those viruses which cause less-frequent disease, such as MVEV. Here we have evaluated the cross-protective values of an inactivated JEV vaccine (JE-VAX) and a live chimeric JEV vaccine (ChimeriVax-JE) against MVEV in two mouse models of flaviviral encephalitis. We show that (i) a three-dose vaccination schedule with JE-VAX provides cross-protective immunity, albeit only partial in the more severe challenge model; (ii) a single dose of ChimeriVax-JE gives complete protection in both challenge models; (iii) the cross-protective immunity elicited with ChimeriVax-JE is durable (≥5 months) and broad (also giving protection against West Nile virus); (iv) humoral and cellular immunities elicited with ChimeriVax-JE contribute to protection against lethal challenge with MVEV; (v) ChimeriVax-JE remains fully attenuated in immunodeficient mice lacking type I and type II interferon responses; and (vi) immunization with JE-VAX, but not ChimeriVax-JE, can prime heterologous infection enhancement in recipients of vaccination on a low-dose schedule, designed to mimic vaccine failure or waning of vaccine-induced immunity. Our results suggest that the live chimeric JEV vaccine will protect against other viruses belonging to the JEV serocomplex, consistent with the observation of cross-protection following live virus infections.
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Ahn, Seon-Jae, Jangsup Moon, Jun-Sang Sunwoo, Jin-Sun Jun, Soon-Tae Lee, Kyung-Il Park, Keun-Hwa Jung, et al. "Respiratory virus-related meningoencephalitis in adults." encephalitis 1, no. 1 (January 10, 2020): 14–19. http://dx.doi.org/10.47936/encephalitis.2020.00052.

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Millichap, J. Gordon. "Herpes Simplex Virus Encephalitis." Pediatric Neurology Briefs 6, no. 4 (April 1, 1992): 27. http://dx.doi.org/10.15844/pedneurbriefs-6-4-3.

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Lee Fanning, W. "Japanese Encephalitis Virus Vaccine." Journal of Travel Medicine 3, no. 1 (March 1, 1996): 57–59. http://dx.doi.org/10.1111/j.1708-8305.1996.tb00698.x.

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Dissertations / Theses on the topic "Virus encephalitis"

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Álvarez, María 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.

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Vander, Kelen Patrick. "Eco-Epidemiology of Eastern Equine Encephalitis Virus." Scholar Commons, 2013. http://scholarcommons.usf.edu/etd/4600.

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ABSTRACT Eastern Equine Encephalitis virus (EEEV) is an alphavirus with high pathogenicity in both humans and horses. Florida continues to have the highest occurrence of human cases in the USA, with four fatalities recorded in 2010. Unlike other states, Florida supports year-round EEEV transmission. This research uses Geographic Information Science (GIS) to examine spatial patterns of documented sentinel seroconversions and horse cases in order to understand the relationships between habitat and transmission intensity of EEEV in Florida. Sentinel sites were categorized as enzootic, periodically enzootic, and negative based on the amount of chicken seroconversions to EEEV. Sentinel sites were analyzed based on land classification data d using the Kruskal-Wallis test to determine which habitats were associated with disease transmission. Cluster analyses were performed for the horse cases using density-based spatial clustering of applications with noise (DBSCAN). Ecological associations of EEEV were examined using compositional analysis and Euclidean distance analysis to determine if the proportion or proximity of certain habitats played a role in transmission. The research in these studies provides evidence of ecological associations for EEEV transmission in Florida that hasn't been previously analyzed. Furthermore, these studies provide the groundwork for better understanding of why there is a disproportionate number of horse and human cases of EEEV in Florida than in any other state.
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Mohammed, 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.

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Japanese encephalitis virus (JEV) is the most important cause of epidemic encephalitis worldwide but its origin is unknown. Epidemics of encephalitis suggestive of Japanese encephalitis (JE) were described in Japan from the 1870s onwards. Four genotypes of JEV have been characterised and representatives of each genotype have been fully sequenced. Based on limited information, a single isolate from Malaysia, the Muar strain, is thought to represent a putative fifth genotype. I have determined the complete nucleotide and amino acid sequence of the Muar strain and compared it with other fully sequenced JEV genomes. Muar was the least similar, with nucleotide divergence ranging from 20.2 to 21.2% and amino acid divergence ranging from 8.5 to 9.9%. Phylogenetic analysis of the Muar strain revealed that it does represent a distinct fifth genotype of JEV. I elucidated the Muar signature amino acids in the envelope (E) protein, including E327 Glutamine on the exposed lateral surface of the putative receptor binding domain of the E protein, which distinguishes the Muar strain from the other four genotypes. Evolutionary analysis of full-length JEV genomes revealed that the mean (range) evolutionary rate is 4.35 x 10-4 (3.4906 X 10-4 to 5.303 x 10-4) nucleotides substitutions per site per year and suggests JEV originated from its ancestral virus in the mid 1500s. It is postulated to have originated in the Indonesia-Malaysia region and evolved there into different genotypes, which then spread across Asia. No strong evidence for positive selection was found between JEV strains of the five genotypes and the E gene has generally been subjected to strong purifying selection. The ability of intravenous immunoglobulins (IVIGs) which sometimes are used as supportive treatment for JEV infection to protect against strains of JEV representing the five major genotypes was assessed. Neutralization assays showed IVIGs appear cross-reactive across the five JEV genotypes with effective but lower titers for the Muar strain as well as representatives from genotype IV. Whether there are other strains from genotype V, and what happened to them remains unknown.
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Tangkanond, 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.

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Vasconcelos, Daphne Y. "The cellular stress response in Measles Virus Encephalitis /." The Ohio State University, 2000. http://rave.ohiolink.edu/etdc/view?acc_num=osu1488194825668105.

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Haglund, Mats. "Tick-borne encephalitis : prognosis, immunization and virus strain characterization /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4453-9/.

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Lindblom, 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.

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Ticks are blood-sucking parasites that are an inconvenience for both humans and animals. The tick by itself is normally harmless unless they attack in excessive numbers. The harm from ticks stems from them being excellent vectors for other parasites, in the form of bacteria and virus that via the ticks are provided a bridge to move across the blood streams of different animals, including humans. One of the most pathogenic tick-borne disease for humans is caused by a flavivirus, the tick-borne encephalitis virus (TBEV). Each year approximately 10 000 individuals on the Eurasian continent develop neurological disease, in the form of meningitis, encephalitis, myelitis and radiculitis, following a bite by a TBEV infected tick. To evaluate the risk of TBEV infection after a tick-bite, we have developed a study to investigate ticks that have bitten humans and to follow up the tick-bitten humans to investigate if they get infected, and if they develop symptoms, and further trace the virus back to the tick that is infected with TBEV. Ticks, blood samples, and questionnaires were collected in collaboration with 34 primary health care centers in Sweden and on the Åland Islands during 2008 and 2009. Several demographical and biological factors were investigated regarding the interaction between ticks and humans. The main finding was that men removed the ticks later than women, and that both older men and older women removed the ticks later than younger individuals. This could in part explain why older individuals in general, and men in particular, are at greater risk of acquiring tick-borne encephalitis (TBE). Furthermore, the prevalence of TBEV in ticks that have bitten humans were investigated, in order to correlate the copy number of TBEV in the tick and the tick feeding-time to the risk of developing symptomatic and asymptomatic infection. This entailed the development of new methodology for tick analysis and TBEV real-time PCR. The result showed a very low risk of TBEV infection in the studied areas, only 5 of 2167 investigated ticks contained TBEV. Three of the individuals bitten by TBEV infected ticks were vaccinated and did not develop symptoms of TBEV infection. One unvaccinated individual got bitten by a tick containing 1800 virus copies, with a feeding-time of 12-24h, and interestingly showed no signs of infection. Another unvaccinated individual got bitten by a tick containing 7.7 million virus copies, with a feedingtime of >60h. This individual developed symptoms consistent with a 1st phase of TBE, including fever and headache, but did not develop the 2nd neurological phase of TBEV infection. Despite only  finding 5 ticks infected with TBEV, a correlation between the virus load in the tick and the tick feeding-time was observed. In 2 other individuals, TBEV antibody seroconversion was detected during the 3 month study period, one without symptoms, while the other experienced symptoms consistent with the 1st phase of TBE. These observations support the hypothesis that a higher virus amount in the tick and a longer feeding time increases the risk of TBEV infection. To further examine TBEV in ticks that have bitten humans and find factors that may predict the risk of human infection and development of TBE, we characterized several TBEV strains genetically. Including TBEV strains isolated from ticks that have bitten human, from questing field-collected ticks, and TBEV strains isolated from patients with TBE. In one of the ticks detached from a human after >60h of feeding, there was a heterogeneous population of TBEV quasispecies with varying poly(A) length in the 3’ untranslated region of the genome was observed. These variations might have implications for differences in virulence between TBEV strains, and the heterogeneous quasispecies population observed could be the virus adapting from replication in tick cells to mammalian cells. We also investigated the response to TBEV vaccination in relation to 14 health-related factors in a population of older individuals on the Åland Islands. Blood samples, questionnaires, and vaccination records were collected from 533 individuals. Three different serological assays to characterize antibody response to TBEV vaccination were used. The main finding was that the number of vaccine doses in relation to age was the most important factor determining successful vaccination. The response to each vaccination dose declined linearly with age, and as much as 47%  of individuals 50 years or older that had taken 3 vaccine doses were seronegative, compared to 23% that had taken 4 doses and 6% with 5 doses. Comparison between the serological assays revealed that the cutoffs determining the balance between sensitivity and specificity differed, but not the overall accuracy. Taken together, these results contribute to a better understanding of the TBEV epidemiology and can provide tools in the prevention of TBE.
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Breakwell, Lucy. "The role of interferon in Semliki Forest virus encephalitis." Thesis, University of Edinburgh, 2006. http://hdl.handle.net/1842/29993.

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This thesis explores the importance of IFN in SFV encephalitis. A quantitative PCR assay for IFN-β and IFN-α transcripts and a quantitative IFN bioassay were developed to determine differences in IFN expression under different infection conditions. Mouse models and primary cell lines were used to establish the importance of PKR for IFN=β expression during SFV infection and to determine whether SFV nsP2 has a role in modulating IFN responses. In the absence of PKR, at early times post-infection, cultured cells reproducibly produced significantly lower levels of IFN-β transcripts. Reduced levels of functional IFN were also demonstrated by bioassay. Previous data has shown that PKR is not required for IFN-β induction. The sensitivity of the qPCR assay has allowed the demonstration that PKR, although not critical for IFN induction, is involved in IFN-β induction and is particularly important at early time points post infection. SFV-nsP2 has been postulated to be involved in IFN interference. Comparing SFV4 to SFV4-nsP2-RDR (a mutant virus with a single amino acid change within the nuclear localisation signal of nsP2, which prevents its translocation into the nucleus) demonstrated that relative to the number of infected cells, the SFV4nsP2-RDR mutant induced over ten –fold more IFN-β transcripts than the wildtype SFV4 strain; this upregulation was specific to IFN-β. The IFN bioassay results supported this data; SFV4-nsP2-RDR induced higher functional IFN levels in comparison to wt SFV4. Both viruses grew to similar titres and at similar rates. In the mutant and wt infections both NF-κB and IRF-3 translocated into the nucleus; however, preliminary EMSA data has suggested that the amount of NF-κB and IRF-3 translocated into the nucleus; however preliminary EMSA data has suggested that the amount of NF-κB bound to the IFN-β promoter is reduced during a wt infection. This suggests a possible mechanism for the differential IFN expression and represents the first IFN evasion mechanism described for an alphavirus.
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Johansen, 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.

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Williams, 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.

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Books on the topic "Virus encephalitis"

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Diamond, Michael S. West Nile Encephalitis Virus Infection. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-0-387-79840-0.

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Booss, John. Viral encephalitis in humans. Washington, D.C: ASM Press, 2003.

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Booss, John. Viral encephalitis in humans. Washington, D.C: ASM Press, 2003.

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Das, Bina Pani. Mosquito Vectors of Japanese Encephalitis Virus from Northern India. India: Springer India, 2013. http://dx.doi.org/10.1007/978-81-322-0861-7.

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Diamond, Michael S. West Nile encephalitis virus infection: Viral pathogenesis and the host immune response. New York, NY: Springer, 2009.

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Jacobs, Susan Catherine. Characterisation and analysis of the NS1 gene of tick-borne encephalitis virus. Oxford: Oxford Brookes University, 1992.

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Murphy, Karen. Helpers simplex virus encephalitis: Establishment and evaluation of the polymerase chain reaction to overcome present diagnostic difficulties. [S.l: The Author], 1995.

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Current issues in clinical neurovirology: Pathogenesis, diagnosis and treatment. Philadelphia, Pa: Saunders, 2008.

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Foley, Paul Bernard. Encephalitis Lethargica: The Mind and Brain Virus. Springer, 2019.

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Foley, Paul Bernard. Encephalitis Lethargica: The Mind and Brain Virus. Springer, 2018.

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Book chapters on the topic "Virus encephalitis"

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Daniels, Peter W., David T. Williams, and John S. Mackenzie. "Japanese Encephalitis Virus." In Trends in Emerging Viral Infections of Swine, 251–63. Ames, Iowa, USA: Iowa State Press, 2008. http://dx.doi.org/10.1002/9780470376812.ch8b.

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Chen, Feng, Dawei Zhao, and Zengxin Jiao. "Nipah Virus Encephalitis." In Radiology of Infectious Diseases: Volume 1, 541–47. Dordrecht: Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-017-9882-2_24.

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Das, Samir, Rahul Kolhe, Arockisamy Arun Prince Milton, and Sandeep Ghatak. "Japanese Encephalitis Virus." In Livestock Diseases and Management, 255–89. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-2651-0_12.

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Pearce, Bradley D. "Encephalitis and Schizophrenia." In Can a Virus Cause Schizophrenia?, 41–66. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9260-4_3.

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Turtle, Lance, and Tom Solomon. "Japanese Encephalitis Virus Infection." In Viral Infections of the Human Nervous System, 271–93. Basel: Springer Basel, 2012. http://dx.doi.org/10.1007/978-3-0348-0425-7_11.

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Bloch, Karen C. "Herpes Simplex and Varicella Zoster Virus." In Meningitis and Encephalitis, 125–40. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-92678-0_9.

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Woods, Steven Paul, and Rodrigo Hasbun. "Human Immunodeficiency Virus (HIV)-Associated CD8 Encephalitis." In Meningitis and Encephalitis, 141–51. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-92678-0_10.

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Petersen, Lyle R. "Global Epidemiology of West Nile Virus." In West Nile Encephalitis Virus Infection, 1–23. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-0-387-79840-0_1.

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Jost, Christiane A., and Theodore C. Pierson. "Antibody-Mediated Neutralization of West Nile Virus: Factors that Govern Neutralization Potency." In West Nile Encephalitis Virus Infection, 219–47. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-0-387-79840-0_10.

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Kuhn, Richard J. "Structural Basis of Antibody Protection Against West Nile Virus." In West Nile Encephalitis Virus Infection, 249–64. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-0-387-79840-0_11.

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Conference papers on the topic "Virus encephalitis"

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Dantas, Madson Caio dos Santos, and João Pedro Cardoso Prudêncio. "Acute cerebellar ataxia associated with varicella zoster virus encephalitis." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.423.

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Context: Varicella-zoster virus (VZV) primary infection causes a diffuse vesicular rash and affects mainly young people. VZV-associated encephalitis is a rare complication since the advent of vaccination, and can present as different neurological syndromes. This report aims to describe a case of acute cerebellar ataxia after VZV-associated encephalitis in a child, admitted to the Onofre Lopes University Hospital (HUOL) in Natal, Brazil. Case report: We present the case of a 9-year-old girl referred to HUOL with polymorphic skin lesions for 8 days. She evolved with headache, vomiting, drowsiness and confusion. Upon admission, she was pale (+/4+), anicteric, confused (GCS=14), hemodynamically stable, SaO2=99%, with pupillary response and no meningism. Laboratory tests showed Hb 11.7g/dl, leukocytes 7,200/mm³ (93% segmented, 1% eosinophils, 5% lymphocytes and 2% monocytes), AST 38U/ml and ALT 46U/ml. Once clinical diagnosis of VZVencephalitis was made, the patient was admitted to the ICU for monitoring and treatment. Cranial CT showed hypodensities on the frontal and occipital lobes; CSF analysis: glucose=76mg/dl, proteins=24mg/dl, leukocytes=9/mm3 (monocytes 78%). She improved progressively and was transferred to the ward, evolving with ataxia, suggesting cerebellitis. Conclusions: This case describes a chickenpox rare complication nowadays: encephalitis. Along evolution, the patient presented acute cerebellar ataxia, a more prevalent condition in children, usually having a limited course.
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Bilasco, Ancuta, Szidonia Florea, Ramona Cirt, Anca Draganescu, Magda Vasile, Camelia Kouris, Cristina Negulescu, and Monica Luminos. "GP45 Autoimmune encephalitis triggered by herpes simplex virus 1 infection." In Faculty of Paediatrics of the Royal College of Physicians of Ireland, 9th Europaediatrics Congress, 13–15 June, Dublin, Ireland 2019. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-epa.111.

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Van Hook, C. J., E. J. McManus, A. Taylor, and B. Warner. "Concurrent Presentation of Transplant Pyelonephritis and West Nile Virus Encephalitis." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1764.

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Yi, Tae Im, Bo Kyoung Kim, and Ji Young Lim. "Neuropsychological and Psychiatric Impairmentafter West Nile Virus Encephalitis-A case report –." In Annual International Conference on Neuroscience and Neurobiology Research. Global Science & Technology Forum (GSTF), 2013. http://dx.doi.org/10.5176/2345-7813_cnn13.11.

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COLLINO, SIMONA, EZIO VENTURINO, LUCA FERRERI, LUIGI BERTOLOTTI, SERGIO ROSATI, and MARIO GIACOBINI. "MODELS FOR TWO STRAINS OF THE CAPRINE ARTHRITIS ENCEPHALITIS VIRUS DISEASE." In 15th International Symposium on Mathematical and Computational Biology. WORLD SCIENTIFIC, 2016. http://dx.doi.org/10.1142/9789813141919_0019.

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Forghani, Majid, Sergey Kovalev, Pavel Vasev, and Mikhail Bolkov. "TBEV Analyzer: a Platform for Evolutionary Analysis of Tick-borne Encephalitis Virus." In 2019 International Multi-Conference on Engineering, Computer and Information Sciences (SIBIRCON). IEEE, 2019. http://dx.doi.org/10.1109/sibircon48586.2019.8958021.

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Vanlandingham, Dana L. "Assessment of risk of a Japanese encephalitis virus introduction in the United States." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.95073.

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Saepulloh, M., N. L. P. I. Dharmayanti, R. M. A. Adjid, A. Ratnawati, and Indrawati Sendow. "The Presence of Japanese Encephalitis Virus Infection in Pteropus sp. in West Kalimantan." In Proceedings of International Seminar on Livestock Production and Veterinary Technology. Indonesian Center for Animal Research and Development (ICARD), 2016. http://dx.doi.org/10.14334/proc.intsem.lpvt-2016-p.549-553.

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Frolenko, V. S., V. I. Uvarova, A. A. Nikitina, E. V. Khvatov, M. Dodina, E. Bayurova, L. I. Kozlovskaya, and D. I. Osolodkin. "SCREENING OF TICK-BORNE ENCEPHALITIS VIRUS METHYLTRANSFERASE INHIBITORS IN VITRO AND IN SILICO." In MedChem-Russia 2021. 5-я Российская конференция по медицинской химии с международным участием «МедХим-Россия 2021». Издательство Волгоградского государственного медицинского университета, 2021. http://dx.doi.org/10.19163/medchemrussia2021-2021-323.

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Lorenzo, Giacchetti, Brunatti Patrizia, Ferrucci Elisabetta, Kottanattu Lisa, Pezzoli Valdo, and Ramelli Gian Paolo. "P76 Respiratory syncytial virus associated acute encephalitis with basal ganglia involvement: a paediatric case report." In 8th Europaediatrics Congress jointly held with, The 13th National Congress of Romanian Pediatrics Society, 7–10 June 2017, Palace of Parliament, Romania, Paediatrics building bridges across Europe. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2017. http://dx.doi.org/10.1136/archdischild-2017-313273.164.

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Reports on the topic "Virus encephalitis"

1

Borucki, M. Eastern Equine Encephalitis Virus. Office of Scientific and Technical Information (OSTI), August 2010. http://dx.doi.org/10.2172/1119926.

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Trent, Dennis W. Development of a Genetically Engineered Venezuelan Equine Encephalitis Virus Vaccine. Fort Belvoir, VA: Defense Technical Information Center, April 1991. http://dx.doi.org/10.21236/ada237590.

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Weilhammer, D. R. Investigating the role of innate immunity in viral encephalitis caused by Rift Valley fever virus. Office of Scientific and Technical Information (OSTI), October 2019. http://dx.doi.org/10.2172/1573140.

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Turell, M. J., C. N. Mores, J. S. Lee, J. J. Paragas, and D. Shermuhemedova. Experimental Transmission of Karshi and Langat (Tick-Borne Encephalitis Virus Complex) Viruses by Ornithodoros Ticks (Acari: Argasidae). Fort Belvoir, VA: Defense Technical Information Center, January 2004. http://dx.doi.org/10.21236/ada428609.

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Jaing, C., and S. Gardner. Interim Report on SNP analysis and forensic microarray probe design for South American hemorrhagic fever viruses, tick-borne encephalitis virus, henipaviruses, Old World Arenaviruses, filoviruses, Crimean-Congo hemorrhagic fever viruses, Rift Valley fever. Office of Scientific and Technical Information (OSTI), June 2012. http://dx.doi.org/10.2172/1044237.

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You might also be interested in the extended bibliographies on the topic 'Virus encephalitis' for particular source types:
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