Academic literature on the topic 'IBDV virus'

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Journal articles on the topic "IBDV virus"

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Sajid, Sanaullah, Sajjad ur Rahman, Mashkoor Mohsin Gilani, Zia ud Din Sindhu, Manel Ben Ali, Amor Hedfi, Mohammed Almalki, and Shahid Mahmood. "Molecular Characterization and Demographic Study on Infectious Bursal Disease Virus in Faisalabad District." PLOS ONE 16, no. 8 (August 16, 2021): e0254605. http://dx.doi.org/10.1371/journal.pone.0254605.

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The re-emergence of virulent strains of the Infectious Bursal Disease Virus (IBDV) leads to significant economic losses of poultry industry in Pakistan during last few years. This disease causes the infection of bursa, which leads to major immune losses. A total number of 30 samples from five IBD outbreaks during the period of 2019–20 were collected from different areas of Faisalabad district, Pakistan and assayed by targeting the IBD virus VP2 region through RT-PCR. Among all the outbreaks, almost 80% of poultry birds were found positive for the IBDV. The bursa tissues were collected from the infected birds and histopathological examination of samples revealed severe lymphocytic depletion, infiltration of inflammatory cells, and necrosis of the bursa of Fabricius (BF). Positive samples were subjected to re-isolation and molecular characterization of IBDV. The Pakistan IBDV genes were subjected to DNA sequencing to determine the virus nucleotide sequences. The sequences of 100 Serotype-I IBDVs showing nearest homology were compared and identified with the study sequence. The construction of the phylogenetic tree for nucleotide sequences was accomplished by the neighbor-joining method in MEGA-6 with reference strains. The VP2 segment reassortment of IBDVs carrying segment A were identified as one important type of circulating strains in Pakistan. The findings indicated the molecular features of the Pakistan IBDV strains playing a role in the evolution of new strains of the virus, which will contribute to the vaccine selection and effective prevention of the disease.
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Pastyria, A., V. Polischuk, and I. Sobko. "GENETIC CHARACTERIZATION OF INFECTIOUS BURSAL DISEASE VIRUS ISOLATES IN UKRAINE." Bulletin of Taras Shevchenko National University of Kyiv. Series: Biology 72, no. 2 (2016): 20–24. http://dx.doi.org/10.17721/1728_2748.2016.72.20-24.

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The objective of the investigation was to characterize infectious bursal disease viruses (IBDV) circulating in commercial poultry farms in Ukraine between 2014 and 2016. IBDV genetic material was amplified directly from bursa. The nucleotide sequence for VP2 hypervariable region of 16 IBDVs were determined by RT-PCR method, sequenced and compared to well characterised IBDV isolates worldwide. Neighbor-joining method was used for phylogenetic analyses. In result of the studyUkrainian IBDVs represented two genetic lineages: very virulent (vv) IBDVs and classical IBDV closely related to attenuated vaccine stains. The nucleotide identity among UkrainianvvIBDVs ranged between 87.2% and 99,8%. Ukrainian vvIBDV strains clustered together with very virulent strains from other counties like: United Kingdom, Egypt, China, Netherlands and Spain. In conclusion this report demonstrates the circulation of vvIBDV in commercial poultry farms in Ukraine.
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Wang, Yulong, Nan Jiang, Linjin Fan, Xinxin Niu, Wenying Zhang, Mengmeng Huang, Li Gao, et al. "Identification and Pathogenicity Evaluation of a Novel Reassortant Infectious Bursal Disease Virus (Genotype A2dB3)." Viruses 13, no. 9 (August 25, 2021): 1682. http://dx.doi.org/10.3390/v13091682.

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Infectious bursal disease virus (IBDV) is a non-enveloped, bi-segmented double-stranded RNA virus and the causative agent of a poultry immunosuppressive disease known as infectious bursal disease (IBD). The novel variant IBDV (nVarIBDV) recently posed a great threat to the development of the poultry industry. In this study, we identified a novel segment-reassortant IBDV strain, IBDV-JS19-14701 (Genotype A2dB3). Phylogenic analysis showed that Segments A and B of IBDV-JS19-14701 were derived from emerging nVarIBDV (Genotype A2dB1) and long-prevalent HLJ0504-like strains (Genotype A3B3) in China, respectively. The pathogenicity of IBDV-JS19-14701 was further evaluated via animal experiments. IBDV-JS19-14701 exhibited a similar virulence to chickens with the nVarIBDV. The identification of this reassortment event is beneficial for understanding the epidemiology of nVarIBDV and will contribute to the efficient prevention and control of IBD.
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Singh, Azad, Megha Bedekar, Rakesh Sharma, Bikash Sarkhel, Sanjeev Singh, and Sudhir Jain. "Detection of very virulent infectious bursal disease virus from a field outbreak in Central India." Acta Veterinaria Hungarica 60, no. 1 (March 1, 2012): 165–74. http://dx.doi.org/10.1556/avet.2012.014.

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In order to detect infectious bursal disease virus (IBDV), bursal tissue was collected from 10 IBD-suspected birds from a 30-day-old, IBDV-vaccinated commercial broiler chicken flock of 2000 birds exhibiting clinical signs suggestive of infectious bursal disease (IBD). The presence of IBDV was confirmed by partial amplification of the VP2 gene by reverse transcription and polymerase chain reaction. Isolates were identified as very virulent strains of IBDV (vvIBDV) by nucleotide sequence analysis. The comparison of the VP2 nucleotide sequences among the isolates revealed the presence of single-nucleotide polymorphisms in the VP2 gene of IBDV in the same flock. The comparative analysis indicated that these viruses were genetically close to the vvIBDVs previously detected in India. Our analysis provided information about the existence of vvIBDV in Central India.
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Alkhalefa, N., M. El-Abasy, S. Kasem, and E. Abu El-Naga. "Molecular characterisation of infectious bursal disease virus (IBDV) isolated from commercial broiler chickens in Nile Delta." BULGARIAN JOURNAL OF VETERINARY MEDICINE 22, no. 4 (2019): 399–408. http://dx.doi.org/10.15547/bjvm.2133.

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Infectious bursal disease virus (IBDV) is a highly infectious disease affecting young chickens that alters predominantly the immune system. Emergence of new variants causes severe economic losses not only in Egypt but also all over the world. For this purpose assessment of infectious bursal disease virus (IBDV) genotypes in 20 commercial broiler flocks aged 20–35 days raised in 5 provinces in the Nile Delta, Egypt (Gharbia, Dakahlya, Kafr El sheikh, Zagazig and Domietta) was carried out. All flocks were vaccinated against IBD virus. RT-PCR revealed successful amplification of 620 bp of VP2 in 17 out of 20 samples (85%). VP2 gene nucleotide sequence analysis of six IBDV isolates (F342-1, F342-2, F342-4, F342-5 and F342-7) revealed 99.1 % similarity to the Giza 2000, Giza 2008 vv, SV-G1, SV-G2, SV-G4 and SV-G5 which were very virulent IBDV strains while the isolate F342-3 was close to D78 classical vaccinal strain and Kal 2001 classical IBDV strain variant.
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Barathidasan, R., S. D. Singh, M. Asok Kumar, P. A. Desingu, M. Palanivelu, M. Singh, and K. Dhama. "Recurrent outbreaks of infectious bursal disease (IBD) in a layer farm caused by very virulent IBD virus (vvIBDV) in India: Pathology and molecular analysis." South Asian Journal of Experimental Biology 3, no. 4 (October 1, 2013): 200–206. http://dx.doi.org/10.38150/sajeb.3(4).p200-206.

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The present study was carried out to investigate and characterize the nature of infectious bursal disease virus (IBDV) involved in the recurrent outbreaks in an experimental layer farm in Bareilly, Uttar Pradesh, India using direct tissue reverse transcription- polymerase chain reaction (RT-PCR) followed by nucleotide sequencing of VP2 gene. A total of three acute IBD outbreaks with the interval of 4-6 months were recorded in the batch of 3-5 weeks-old layer chicks in the year 2012-2013. Tissues collected from necropsied birds were found RT-PCR positive for IBDV VP2 gene. Genetic analysis of the sequenced VP2 gene revealed the IBDV belonged to very virulent (vv) subtype and had amino acids at positions 222A, 256I, 294I, and 299S typical for vvIBDV strains isolated worldwide. It had only one unique amino acid change in the antigenic peak A (210-225 aa) at position 212DàN (AspàAsn), which is not observed in any of the vvIBDVs isolated in India and abroad. Phylogenetic analysis revealed the isolates were more closely related to vvIBDV strains rA and rB (U.S.A.), Gx and HLJ-7 (China), OKYM (Japan), and shared >95% nucleotide homology with them. The VP2 gene shared 96.7% amino acid homology with IBDI+ vaccine strain used in India, comparatively higher among other vaccines strains, suggesting that IBD intermediate plus (IBDI+) vaccine might provide optimum cross protection, also for other vvIBDV strains. The vvIBDV strains remain a threat to poultry industry worldwide, and require regular monitoring and genetic analysis in order to keep track of the appearance and evolution of antigenically different IBDV strains or subtypes.
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Saha, PK, MH Ali, MB Rahman, and MA Islam. "DETERMINATION OF SENSITIVITY AND SPECIFICITY OF IN-HOUSE SANDWICH ELISA FOR THE DETECTION OF INFECTIOUS BURSAL DISEASE VIRUSES." Bangladesh Journal of Veterinary Medicine 8, no. 2 (July 11, 2012): 97–106. http://dx.doi.org/10.3329/bjvm.v8i2.11185.

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The study was designed for the development of an In-House sandwich ELISA as a suitable serological method for the rapid detection of infectious bursal disease virus (IBDV). The test was also designed to compare and evaluate its sensitivity and specificity with other traditional methods used for the detection of IBDV from field outbreak cases prevalent among the poultry population of Bangladesh. To develop the In-House sandwich ELISA, hyper-immune serum was raised against live IBDV vaccine in rabbit which was used to coat each of the 96-well flat bottomed polystyrene microtitre plate whereas, hyper-immune sera raised in chickens against IBDV used as secondary antibody. The newly developed In-House sandwich ELISA was standardized by dispensing different dilutions (10-1 up to 10-4) of rabbit serum. Among them, the 10-2 dilution of serum showed most suitable reading for the detection of IBD virus and used to coat the plate to evaluate its sensitivity and specificity. Sensitivity test was done by different dilutions (10-0 to 10-4) of reference IBD virus. The virus dilution, 10-3 was the highest dilution having lowest capacity to bind with coated antibody of the ELISA plate which indicated that IBD viruses was absent in the dilutions of above 10-3. The cut-off value of negative control samples was determined as 0.937 which indicated titer of tested samples >0.937 was positive and <0.937 was negative. Specificity test was performed using different known viruses (IBDV and NDV) using different dilutions (10-1 up to 10-4). Only the IBDV showed positive result which indicated high specificity of newly developed ELISA plate. A total of 26 samples (feces, cloacal swab, spleen and bursa) from control group, experimental and natural IBDV outbreaks were used as field viral antigen for the evaluation of sensitivity and specificity of the newly developed In-House sandwich ELISA. In case of experimental infection, 5 (62.5%) of 8 feces sample but none of cloacal swab were positive for IBDV whereas, all bursa and spleen samples were positive by both In–House sandwich ELISA and AGIDT. In case of natural outbreak cases, 6 of 6 bursal samples and 4 of 6 spleen samples were positive by In-House sandwich ELISA whereas, AGIDT detected all bursal and 3 spleen samples. No virus was detected from the samples of control group. The result showed 92.85% specificity of the developed sandwich ELISA for detection of IBDV with AGIDT which indicated that the developed ELISA is a sensitive, specific, cost effective and reliable tool for the detection of IBDV antigen from a large number of field samples.DOI = http://dx.doi.org/10.3329/bjvm.v8i2.11185 Bangl. J. Vet. Med. (2010). 8 (2) : 97-106
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Tao, Qimeng, Xiurong Wang, Hongmei Bao, Jianan Wu, Lin Shi, Yanbing Li, Chuanling Qiao, Samuilenko Anatolij Yakovlevich, Poukhova Nina Mikhaylovna, and Hualan Chen. "Detection and Differentiation of Four Poultry Diseases Using Asymmetric Reverse Transcription Polymerase Chain Reaction in Combination with Oligonucleotide Microarrays." Journal of Veterinary Diagnostic Investigation 21, no. 5 (September 2009): 623–32. http://dx.doi.org/10.1177/104063870902100506.

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Asymmetric reverse transcription polymerase chain reaction (RT-PCR) and microarrays were combined to distinguish 4 viruses, including Avian influenza virus (AIV), Newcastle disease virus (NDV), Infectious bronchitis virus (IBV), and Infectious bursal disease virus (IBDV), and hemagglutinin (HA) subtypes H5, H7, and H9, and neuraminidase (NA) subtypes N1 and N2 of AIV. The AIV matrix protein (M), and HA and NA genes, IBV nucleoprotein (NP) gene, NDV NP gene, and IBDV A fragment gene were cloned into plasmids. These genes were amplified from these positive recombinant plasmids, which included the inserted target genes by PCR. The PCR products were purified and printed on the amino-modified slides as the probes. RNA was extracted from samples and labeled by asymmetric RT-PCR using a cyanine (Cy)3–labeled primers. The labeled complementary (c)DNA was hybridized to the probes immobilized on the glass slides. After hybridization, the microarrays were scanned, and the hybridization pattern agreed perfectly with the known location of each probe. No cross-hybridization could be detected. Results demonstrated that microarray based on asymmetric RT-PCR is an effective way to distinguish AIV, IBV, NDV, and IBDV simultaneously.
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González, Dolores, Jose Francisco Rodríguez, and Fernando Abaitua. "Intracellular Interference of Infectious Bursal Disease Virus." Journal of Virology 79, no. 22 (November 15, 2005): 14437–41. http://dx.doi.org/10.1128/jvi.79.22.14437-14441.2005.

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ABSTRACT A search for dominant-negative mutant polypeptides hampering infectious bursal disease virus (IBDV) replication has been undertaken. We have found that expression of a mutant version of the VP3 structural polypeptide known as VP3/M3, partially lacking the domain responsible for the interaction with the virus-encoded RNA polymerase, efficiently interferes with the IBDV replication cycle. Transformed cells stably expressing VP3/M3 show a significant reduction (up to 96%) in their ability to support IBDV growth. Our findings provide a new tool for the characterization of the IBDV replication cycle and might facilitate the generation of genetically modified chicken lines with a reduced susceptibility to IBDV infection.
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Li, Jiaxin, and Shijun J. Zheng. "Role of MicroRNAs in Host Defense against Infectious Bursal Disease Virus (IBDV) Infection: A Hidden Front Line." Viruses 12, no. 5 (May 14, 2020): 543. http://dx.doi.org/10.3390/v12050543.

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Infectious bursal disease (IBD) is an acute, highly contagious and immunosuppressive avian disease caused by infectious bursal disease virus (IBDV). In recent years, remarkable progress has been made in the understanding of the pathogenesis of IBDV infection and the host response, including apoptosis, autophagy and the inhibition of innate immunity. Not only a number of host proteins interacting with or targeted by viral proteins participate in these processes, but microRNAs (miRNAs) are also involved in the host response to IBDV infection. If an IBDV–host interaction at the protein level is taken imaginatively as the front line of the battle between invaders (pathogens) and defenders (host cells), their fight at the RNA level resembles the hidden front line. miRNAs are a class of non-coding single-stranded endogenous RNA molecules with a length of approximately 22 nucleotides (nt) that play important roles in regulating gene expression at the post-transcriptional level. Insights into the roles of viral proteins and miRNAs in host response will add to the understanding of the pathogenesis of IBDV infection. The interaction of viral proteins with cellular targets during IBDV infection were previously well-reviewed. This review focuses mainly on the current knowledge of the host response to IBDV infection at the RNA level, in particular, of the nine well-characterized miRNAs that affect cell apoptosis, the innate immune response and viral replication.
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Dissertations / Theses on the topic "IBDV virus"

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Lüken, Caroline. "Untersuchungen zur Apoptoseinduktion des Virus der Infektiösen Bursitis (IBDV)." Doctoral thesis, Universitätsbibliothek Leipzig, 2009. http://nbn-resolving.de/urn:nbn:de:bsz:15-20090224-072016-6.

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Das Virus der infektiösen Bursitis (IBDV) gehört dem Genus Avibirnavirus der Familie Birnaviridae an. Die infektiöse Bursitis ist eine bedeutende, weltweit verbreitete Erkrankung des Geflügels. IBDV beinhaltet zwei verschiedene Serotypen: Serotyp 1 und 2. Serotyp 2 ist apathogen und wurde aus dem Respirationstrakt von Puten isoliert. Serotyp 1 ist pathogen für Hühner. Innerhalb des Serotyp 1 unterscheidet man klassisch virulente (cv), hochvirulente (hv) Stämme und Variantstämme. Während cv- und hv-Stämme zu nekrotisch-hämorrhagischen Entzündungen der Bursa Fabricii führen, verursachen Variantstämme eine sehr rasche Atrophie dieses Organs. Daher liegt die Annahme nahe, dass die Variantstämme ein besonders hohes Potenzial zur Apoptoseinduktion besitzen. Diese Hypothese war grundlegend für die Fragestellungen und Zielsetzungen dieser Arbeit. Zur Generierung infektiöser Viren mittels reverser Genetik wurden im Zuge dieser Arbeit zunächst „Volle-Länge-Plasmide“ beider Segmente des Variantstamms Variant E hergestellt. Vor das 5`-Ende der IBDV-spezifischen Sequenz wurde ein T7-Promotor kloniert, am 3`-Ende besitzt das „Volle- Länge-Plasmid“ eine Restriktionsenzymschnittstelle zur Linearisierung. Mittels „QuikChange“-PCR wurden die für die Zellkulturadaptation benötigten Punktmutationen in die VP2-codierende Region des Segments A eingefügt. Nach der Sequenzierung wurden, ebenfalls mittels „QuikChange“-PCR, unerwünschte Mutationen in beiden Segmenten revertiert. Mittels in vitro-Transkription wurde die cDNA der „Volle-Länge-Plasmide“ von Segment A und B des Variant E-Stamms und Segment B des klassisch virulenten Stammes Cu-1 in cRNA umgeschrieben. Durch Cotransfektion verschiedener Kombinationen von cRNA in HEF wurde ein zellkulturadaptiertes reassortantes Virus, bestehend aus Segment A von Variant E und Segment B von Cu-1 generiert. Dieses wurde als Var E A/Cu-1 B bezeichnet. Nach drei aufeinander folgenden Passagen in HEF wurden die infektiösen Nachkommen geerntet und durch RT-PCR, Sequenzierung, Restriktionsenzymanalyse (REA), indirekten Immunfluoreszenztest (IIFT) und Western blot charakterisiert. Durch Elektronenmikroskopie wurden die typischen morphologischen Merkmale von IBDV nachgewiesen. Durch Ermittlung einer Wachstumskinetik zeigte sich, dass das Virus im Vergleich zu zellkulturadaptiertem Cu-1 eine langsamere Vermehrung aufwies, jedoch einen annähernd gleichen Virustiter erreichte. Zum Nachweis von Apoptose wurden infizierte HEF zu definierten Zeitpunkten geerntet und im DNA-Laddering-Versuch und im Caspase-Glo 3/7 Assay untersucht. Dabei wurde die an HEF adaptierte Reassortante Var E A/Cu-1 B mit dem klassisch virulenten Stamm Cu-1 hinsichtlich des Potenzials zur Apoptoseinduktion verglichen. Die Anwesenheit der viralen Polymerase VP1 von Cu-1 in beiden Viren ließ einen direkten Vergleich der von dem Segment A codierten, für die Apoptose verantwortlichen Proteine VP2 und VP5 beider Stämme zu. Durch diese Experimente wurde deutlich, dass die Reassortante Var E A/Cu-1 B im Vergleich zu Cu-1 eine schwächere Fähigkeit zur Apoptoseinduktion zeigt. Dieses unerwartete Ergebnis kann mit der Verwendung zellkulturadaptierter Viren mit reduzierter Virulenz, einer geringeren Replikationsgeschwindigkeit der Reassortanten und/oder der Verwendung eines nichtwirtszellspezifischen Zellkultursystems zu begründen sein. Weiterführende Untersuchungen in vivo, unter Einbeziehung des Elternstamms Variant E, wären daher von Interesse. VP5 wurde von mehreren Arbeitsgruppen als ein apoptoseauslösendes Protein identifiziert. Andere Studien ergaben jedoch auch, dass VP5 in frühen Stadien der Infektion Apoptose inhibiert. Vergleiche einer in dieser Arbeit generierten VP5-Deletionsmutante mit Cu-1 sollten daher klären, wie sich eine VP5-Deletion bei einem gut untersuchten, zellkulturadaptierten, klassisch virulenten Stamm auf die Induktion von Apoptose auswirkt. Die Cu-1 VP5-Deletionsmutante zeigte, trotz verminderter Replikationsgeschwindigkeit, in den Anfangsstadien der Infektion ein erhöhtes apoptotisches Potenzial. Daraus lässt sich schließen, dass VP5 eine inhibierende Wirkung auf die Apoptose besitzt. Möglicherweise liegt der biologische Grund darin, dass sich IBDV in den Anfangsstadien der Infektion durch die VP5-inhibierte Apoptose besser vermehren kann.
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Xue, Chunyi, and 薛春宜. "Molecular characterization of infectious bursal disease virus (IBDV) receptor." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B31246187.

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Wark, Kim Louise. "Expression and processing of infectious bursal disease virus proteins." Thesis, University of Hertfordshire, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.323651.

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Wong, Tsz-yeung, and 王子揚. "IBDV-mediated antiviral responses by TLR3 signaling pathways." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B41897201.

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Wong, Tsz-yeung, and 王子揚. "Molecular characterization of IBDV-induced apoptosis in vitro using cDNA microarrays." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B36375998.

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Zenkina, Olga. "Etablierung eines Zellkultursystems zur Isolierung hochvirulenter Stämme des Virus der infektiösen Bursitis (IBDV)." Doctoral thesis, Universitätsbibliothek Leipzig, 2009. http://nbn-resolving.de/urn:nbn:de:bsz:15-20091019-093926-5.

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Die Infektiöse Bursitis ist eine Virusinfektion 3-6 Wochen alter Hühner, die bei Überlebenden mit einer schweren Immunsuppression verbunden ist. Sie verursacht weltweit große wirtschaftliche Schäden. Seit dem Auftreten hoch virulenter (hv) Stämme des Virus der infektiösen Bursits (infectious bursal disease virus, IBDV) Ende der 80-er Jahre blieben viele Fragen zu den biologischen Eigenschaften dieser Virusstämme und einer effektiven Bekämpfung der von ihnen ausgelösten Erkrankung ungeklärt. Unter anderem gelingt es zumeist nicht, hv-Stämme in der Zellkultur zu isolieren. Von besonderem Interesse ist es daher, solche Zellkulturen zu erhalten, die es erlauben, hv-Stämme in vitro zu züchten, ohne dass zuvor deren Genom verändert werden muss. Ziel dieser Arbeit war es daher, geeignete Zellkulturen für die Vermehrung von hv-IBDV-Stämmen zu etablieren und dann einige von deren biologischen Eigenschaften näher zu untersuchen.
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Sachs, Katja. "Expression von Proteinen des Virus der infektiösen Bursitis (IBDV) mit Hilfe rekombinanter Influenzaviren." Doctoral thesis, Universitätsbibliothek Leipzig, 2005. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-34094.

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Hot, David P. O. "Expression and characterisation of the polymerase (VP1) of Infectious Bursal Disease Virus (IBDV)." Thesis, University of Reading, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297639.

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Rudd, Matthew Francis, and mikewood@deakin edu au. "Virulence determinants of infectious bursal disease virus." Deakin University. School of Biological and Chemical Sciences, 2003. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20050825.103742.

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The very virulent (vv) pathotype of infectious bursal disease virus (IBDV) has spread rapidly throughout Europe, Asia, and the Middle East. Although Australia is currently unaffected, there remains the potential for incursion of an exotic isolate. The aim of this study was to identify putative virulence determinants of IBDV to facilitate the development of improved diagnostic assays for detection and characterisation of vvIBDV isolates. Sequencing of Indonesian vvIBDV Tasik94 revealed a unique substitution [ A¨S222] in the hypervariable region (HVR) of viral protein (VP) VP2, which did not appear to impinge on virulence or antigenicity. Phylogenetic analyses indicated that Tasik94 was closely related to Asian and European vvIBDV strains. Extensive alignment of deduced protein sequences across the HVR of VP2 identified residuesI242 I256 and I294 as putative markers of the vv phcnotype. Comparison of the pathology induced by mildly-virulent Australian IBDV 002/73 and Indonesian vvIBDV Tasik94, revealed that histological lesions in the spleen, thymus and bone marrow were restricted to Tasik94-infected birds, suggesting the enhanced pathogenicity of vvIBDV might be attributed to replication in non-bursal lymphoid organs. The biological significance of the VP2 HVR in virulence was assessed using recombinant viruses generated by reverse genetics. Both genomic segments of Australian IBDV 002/73, and recombinant segment A constructs in which the HVR of 002/73 was replaced with the corresponding region of either tissue culture-adapted virus or vvIBDV (Tasik94), were cloned behind T7 RNA polymerase promoter sequences. In vitro transcription/translation of each construct resulted in expression of viral proteins. Co-transfection of synthetic RNA transcripts initiated replication of both tissue culture-adapted parental and recombinant viruses, however attempts to rescue non-adapted viruses in specific-pathogen-free (SPF) chickens were unsuccessful. Nucleotide sequence variation in the HVR of VP2 was exploited for the development of a new diagnostic assay to rapidly detect exotic IBDV isolates, including vvIBDV, using reverse transcription polymerase chain reaction (RT-PCR) amplification and Bmrl restriction enzyme digestion. The assay was capable of differentiating between endemic and exotic IBDV in 96% of 105 isolates sequenced to date.
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Rauf, Abdul. "PERSISTENCE, DISTRIBUTION AND IMMUNOPATHOGENESIS OF INFECTIOUS BURSAL DISEASE VIRUS IN CHICKENS." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1299612513.

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Book chapters on the topic "IBDV virus"

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Hemida, Maged Gomaa, Abdullah I. A. Al-Mubarak, Adel M. Abdelaziz, and Abdulazim M. Ibrahim. "Infectious Bursal Disease Virus (IBDV)." In Recent Advances in Animal Virology, 237–52. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-9073-9_13.

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Tomley, Fiona, Matthew Binns, Mike Boursnell, and Adrian Mockett. "Expression of IBV Spike Protein by a Vaccinia Virus Recombinant." In Coronaviruses, 151–53. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-1280-2_17.

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Stirrups, Kathleen, Kathleen Shaw, Sharon Evans, Kevin Dalton, David Cavanagh, and Paul Britton. "Rescue of IBV D-RNA by Heterologous Helper Virus Strains." In Advances in Experimental Medicine and Biology, 259–64. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5331-1_33.

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Kit, Saul, Malon Kit, Richard DiMarchi, Sheila Little, and Charles Gale. "Modified-Live Infectious Bovine Rhinotracheitis Virus (IBRV) Vaccine Expressing Foot-and-Mouth Disease Virus (FMDV) Capsid Protein Epitopes on Surface of Hybrid Virus Particles." In Advances in Experimental Medicine and Biology, 211–20. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-6000-1_23.

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Shen, Shuo, and Ding Xiang Liu. "Characterization of Temperature-sensitive (ts) Mutants of Coronavirus Infectious Bronchitis Virus (IBV)." In Advances in Experimental Medicine and Biology, 557–62. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1325-4_82.

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Penzes, Zoltan, Kefford W. Tibbles, Kathy Shaw, Paul Britton, T. David K. Brown, and David Cavanagh. "Generation of a Defective RNA of Avian Coronavirus Infectious Bronchitis Virus (IBV)." In Advances in Experimental Medicine and Biology, 563–69. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1899-0_90.

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Wilson, T. J., K. Mitrangas, H. C. Ramm, R. L. Boyd, and H. A. Ward. "Response of the Chicken Bursal Stroma to Treatment with Cyclophosphamide and IBD Virus." In Advances in Experimental Medicine and Biology, 75–80. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-5535-9_10.

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Liu, D. X., S. Shen, H. Y. Xu, and T. D. K. Brown. "Proteolytic Processing of the Polyprotein Encoded by ORF1b of the Coronavirus Infectious Bronchitis Virus (IBV)." In Advances in Experimental Medicine and Biology, 149–59. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5331-1_20.

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Lim, K. P., H. Y. Xu, and D. X. Liu. "Physical Interaction Between the Membrane (M) and Envelope (E) Proteins of the Coronavirus Avian Infectious Bronchitis Virus (IBV)." In Advances in Experimental Medicine and Biology, 595–602. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1325-4_88.

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Liu, D. X., H. Y. Xu, and K. P. Lim. "Regulation of mRNA 1 Expression by the 5’-Untranslated Region (5’-UTR) of the Coronavirus Infectious Bronchitis Virus (IBV)." In Advances in Experimental Medicine and Biology, 303–11. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5331-1_40.

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Conference papers on the topic "IBDV virus"

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Elbashir, Israa, Heba Al Khatib, and Hadi Yassine. "Replication Dynamics, Pathogenicity, and Evolution of Influenza Viruses in Intestinal Caco-2 Cells." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0166.

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Abstract:
Background: Influenza virus is a major cause of respiratory infections worldwide. Besides the common respiratory symptoms, namouras cases with gastrointestinal symptoms have been reported. Moreover, influenza virus has been detected in feces of up to 20.6 % of influenza-infected patients. Therefore, direct infection of intestinal cells with influenza virus is suspected; however, the mechanism of this infection has not been explored. AIM: To investigate influenza virus replication, cellular responses to infection, and virus evolution following serial infection in human Caucasian colon adenocarcinoma cells (Caco-2 cells). Method: Two influenza A subtypes (A/H3N2 and A/H1N1pdm 09) and one influenza B virus (B/Yamagata) were serially passaged in Caco-2. Quantitative PCR was used to study hormones and cytokines expression following infection. Deep sequencing analysis of viral genome was used to assess the virus evolution. Results: The replication capacity of the three viruses was maintained throughout 12 passages, with H3N2 virus being the fastest in adaptation. The expression of hormone and cytokines in Caco-2 cells was considerably different between the viruses and among the passages, however, a pattern of induction was observed at the late phase of infection. Deep sequencing analysis revealed a few amino acid substitutions in the HA protein of H3N2 and H1N1 viruses, mostly in the antigenic site. Moreover, virus evolution at the quasispecies level based on HA protein revealed that H3N2 and H1N1 harbored more diverse virus populations when compared to IBV, indicating their higher evolution within Caco-2 cells. Conclusion: The findings of this study indicate the possibility of influenza virus replication in intestinal cells. To further explain the gastrointestinal complications of influenza infections in-vivo experiments with different influenza viruses are needed.
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