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1
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 InHouse 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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GEORGOPOULOU (Ι. ΓΕΩΡΓΟΠΟΥΛΟΥ), J. "Gumboro disease (IBD)." Journal of the Hellenic Veterinary Medical Society 56, no. 1 (November 29, 2017): 59. http://dx.doi.org/10.12681/jhvms.15072.
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Gumboro Disease (IBD) caused by Infectious Bursal Disease Virus is an immunosuppressive condition of chickens, which resulted in severe economical losses. Approximately 47 years after the first appearance of the disease, the changes in the form of presentation and pathogenicity of IBDV in the field has resulted in continual changes and adjustments of the vaccines used to control IBD. The original form of the disease, also known as classic or clinical IBD, was usually observed after the third week of life with high mortality, depending on factors, such as virulence of the strain of virus involved, age of the birds and maternal antibody status. The acute IBD is caused by the very virulent IBDV strains, characterized by high mortality rates in vaccinated chickens and the clinical signs and lesions are similar to those of the classic form. The subclinicalform of the disease is associated with the "variant" strains of IBDV and is characterized by low mortality and severe immunosuppression. Initially, the classic IBD was controlled by the use of mild vaccines produced in the early 1970s and from the late 1980s revealed absence of protection from wIBDV in vaccinated chickens. Another group of vaccinal strains, known as intermediate plus vaccine, has been used to control wIBDV strains. These vaccines multiply in birds, even in the presence of high maternal antibody titers. In the USA and other countries, the disease from the variant strains was controlled by intermediate strains as well as by inactivated vaccines that included variant strains, thus providing maternal antibodies against both the standard and variant strains. Until today, the IBD continues to pose an important threat to commercial poultry industry. The high resistence of IBDV to physical and chemical agents accounts for persistence of the virus in the outside environment, particularly on contaminated farms, despite disinfection. Nevertheless and not quite unexpected for the IBDV mutations in the genome, resulted in the emergence of antigenic variant strains in vaccinated flocks. The IBD requires heightened vigilance and the incidence and prevalence of the clinical and immunosuppressive forms must be evaluated more precisely.
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Huang, Zhuhui, Subbiah Elankumaran, Abdul S. Yunus, and Siba K. Samal. "A Recombinant Newcastle Disease Virus (NDV) Expressing VP2 Protein of Infectious Bursal Disease Virus (IBDV) Protects against NDV and IBDV." Journal of Virology 78, no. 18 (September 15, 2004): 10054–63. http://dx.doi.org/10.1128/jvi.78.18.10054-10063.2004.
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ABSTRACT Infectious bursal disease virus (IBDV) causes a highly immunosuppressive disease in chickens. Currently available, live IBDV vaccines can lead to generation of variant viruses. We have developed an alternative vaccine that will not create variant IBDV. By using the reverse genetics approach, we devised a recombinant Newcastle disease virus (NDV) vector from a commonly used vaccine strain LaSota to express the host-protective immunogen VP2 of a variant IBDV strain GLS-5. The gene encoding the VP2 protein of the IBDV was inserted into the most 3′-proximal locus of a full-length NDV cDNA for high-level expression. We successfully recovered the recombinant virus, rLaSota/VP2. The rLaSota/VP2 was genetically stable, at least up to 12 serial passages in chicken embryos, and was shown to express the VP2 protein. The VP2 protein was not incorporated into the virions of recombinant virus. Recombinant rLaSota/VP2 replicated to a titer similar to that of parental NDV strain LaSota in chicken embryos and cell cultures. To assess protective efficacy of the rLaSota/VP2, 2-day-old specific-pathogen-free chickens were vaccinated with the recombinant virus and challenged with a highly virulent NDV strain Texas GB or IBDV variant strain GLS-5 at 3 weeks postvaccination. Vaccination with rLaSota/VP2 generated antibody responses against both NDV and IBDV and provided 90% protection against NDV and IBDV. Booster immunization induced higher levels of antibody responses against both NDV and IBDV and conferred complete protection against both viruses. These results indicate that the recombinant NDV can be used as a vaccine vector for other avian pathogens.
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Lombardo, Eleuterio, Antonio Maraver, José R. Castón, José Rivera, Armando Fernández-Arias, Antonio Serrano, José L. Carrascosa, and José F. Rodriguez. "VP1, the Putative RNA-Dependent RNA Polymerase of Infectious Bursal Disease Virus, Forms Complexes with the Capsid Protein VP3, Leading to Efficient Encapsidation into Virus-Like Particles." Journal of Virology 73, no. 8 (August 1, 1999): 6973–83. http://dx.doi.org/10.1128/jvi.73.8.6973-6983.1999.
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ABSTRACT A cDNA corresponding to the coding region of VP1, the putative RNA-dependent RNA polymerase, of infectious bursal disease virus (IBDV) was cloned and inserted into the genome of a vaccinia virus inducible expression vector. The molecular mass and antigenic reactivity of VP1 expressed in mammalian cells are identical to those of its counterpart expressed in IBDV-infected cells. The results presented here demonstrate that VP1 is efficiently incorporated into IBDV virus-like particles (VLPs) produced in mammalian cells coexpressing the IBDV polyprotein and VP1. Incorporation of VP1 into VLPs requires neither the presence of IBDV RNAs nor that of the nonstructural polypeptide VP5. Immunofluorescence, confocal laser scanning microscopy, and immunoprecipitation analyses conclusively showed that VP1 forms complexes with the structural polypeptide VP3. Formation of VP1-VP3 complexes is likely to be a key step for the morphogenesis of IBDV particles.
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Kim, In-Jeong, Seung Kwon You, Hyungee Kim, Hung-Yeuh Yeh, and Jagdev M. Sharma. "Characteristics of Bursal T Lymphocytes Induced by Infectious Bursal Disease Virus." Journal of Virology 74, no. 19 (October 1, 2000): 8884–92. http://dx.doi.org/10.1128/jvi.74.19.8884-8892.2000.
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ABSTRACT Infectious bursal disease virus (IBDV) is an avian lymphotropic virus that causes immunosuppression. When specific-pathogen-free chickens were exposed to a pathogenic strain of IBDV (IM), the virus rapidly destroyed B cells in the bursa of Fabricius. Extensive viral replication was accompanied by an infiltration of T cells in the bursa. We studied the characteristics of intrabursal T lymphocytes in IBDV-infected chickens and examined whether T cells were involved in virus clearance. Flow cytometric analysis of single-cell suspensions of the bursal tissue revealed that T cells were first detectable at 4 days postinoculation (p.i.). At 7 days p.i., 65% of bursal cells were T cells and 7% were B cells. After virus infection, the numbers of bursal T cells expressing activation markers Ia and CD25 were significantly increased (P < 0.03). In addition, IBDV-induced bursal T cells produced elevated levels of interleukin-6-like factor and nitric oxide-inducing factor in vitro. Spleen and bursal cells of IBDV-infected chickens had upregulated gamma interferon gene expression in comparison with virus-free chickens. In IBDV-infected chickens, bursal T cells proliferated in vitro upon stimulation with purified IBDV in a dose-dependent manner (P < 0.02), whereas virus-specific T-cell expansion was not detected in the spleen. Cyclosporin A treatment, which reduced the number of circulating T cells and compromised T-cell mitogenesis, increased viral burden in the bursae of IBDV-infected chickens. The results suggest that intrabursal T cells and T-cell-mediated responses may be important in viral clearance and promoting recovery from infection.
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Yang, Bo, Nana Yan, Aijing Liu, Yue Li, Zehua Chen, Li Gao, Xiaole Qi, et al. "Chicken eEF1α is a Critical Factor for the Polymerase Complex Activity of Very Virulent Infectious Bursal Disease Virus." Viruses 12, no. 2 (February 23, 2020): 249. http://dx.doi.org/10.3390/v12020249.
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Infectious bursal disease (IBD) is an immunosuppressive, highly contagious, and lethal disease of young chickens caused by IBD virus (IBDV). It results in huge economic loss to the poultry industry worldwide. Infection caused by very virulent IBDV (vvIBDV) strains results in high mortality in young chicken flocks. However, the replication characteristics of vvIBDV are not well studied. Publications have shown that virus protein 3 (VP3) binds to VP1 and viral double-stranded RNA, and together they form a ribonucleoprotein complex that plays a key role in virus replication. In this study, vvIBDV VP3 was used to identify host proteins potentially involved in modulating vvIBDV replication. Chicken eukaryotic translation elongation factor 1α (cheEF1α) was chosen to further investigate effects on vvIBDV replication. By small interfering RNA-mediated cheEF1α knockdown, we demonstrated the possibility of significantly reducing viral polymerase activity, with a subsequent reduction in virus yields. Conversely, over-expression of cheEF1α significantly increased viral polymerase activity and virus replication. Further study confirmed that cheEF1α interacted only with vvIBDV VP3 but not with attenuated IBDV (aIBDV) VP3. Furthermore, the amino acids at the N- and C-termini were important in the interaction between vvIBDV VP3 and cheEF1α. Domain III was essential for interactions between cheEF1α and vvIBDV VP3. In summary, cheEF1α enhances vvIBDV replication by promoting the activity of virus polymerase. Our study indicates cheEF1α is a potential target for limiting vvIBDV infection.
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PIKUŁA, ANNA, and KRZYSZTOF ŚMIETANKA. "Selected aspects of infectious bursal disease – the current state of knowledge." Medycyna Weterynaryjna 74, no. 10 (2023): 6138–2023. http://dx.doi.org/10.21521/mw.6138.
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Infectious bursal disease (IBD) is a highly infectious and contagious immunosuppressive viral disease of chickens with a worldwide economic significance to the poultry industry. Over fifty years have passed since the first confirmed occurrence of the disease, and the virus has spread all over world and evolved into multiple genetic, antigenic and pathotypic variants, becoming a serious threat to the poultry industry. The primary tool in IBD eradication is the maintenance of strict biosecurity in poultry farms and implementation of vaccination programmes which should take into account the current epidemiological knowledge about the IBDV strains circulating in the field. This review article presents the current state of knowledge about the infectious bursal disease virus (IBDV) with special regard to the molecular biology of the virus, immunological aspects, as well as current and future prevention strategies.
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Abbas, Ali Hadi, Haider Abas AL saegh, and Furkan Sabbar ALaraji. "Sequence diversity and evolution of infectious bursal disease virus in Iraq." F1000Research 10 (April 16, 2021): 293. http://dx.doi.org/10.12688/f1000research.28421.1.
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Background: Infectious Bursal Disease (IBD) is a highly infectious disease which causes huge economic losses to the poultry industry due to the direct impact of the illness and indirect consequences such as decreasing the general immunity of the flock, leaving it naive to other diseases. In Iraq, IBD is highly prevalent despite vaccination programs, yet studies on sequence diversity of the causative virus are still rare. Methods: A sample from Bursa of Fabricius from an IBD outbreak in a flock in the city of Najaf in Iraq was smeared on an FTA card. Amplicons of targeted regions in VP1 and VP2 genes were generated and sequenced. Sequences were then compared with other local and global sequences downloaded from GenBank repositories. Sequence alignment and DNA sequence analyses were achieved using MUSCLE, UGENE and MEGAx software. The molecular clock and sequence evolutionary analyses were applied using MEGAx tools. Results: The strain sequenced in this study belongs to a very virulent Infectious Bursal Disease Virus (vvIBDV) as the DNA and phylogenetic analysis of VP1 and VP2 gene sequences showed a mutual clustering with similar sequences belonging to vvIBDV genogroup 3. Analyses of the hyper variable region of VP2 gene (hvVP2) of IBDV isolates from Iraq indicates a presence of sequence diversity. Interestingly, the two vaccine strains Ventri IBDV Plus and ABIC MB71 that showed the highest sequence similarity to the local isolates in the hvVP2 region are not used in vaccination routine against IBDV in Iraq. Conclusion: Sequences of vvIBDV in Iraq are diverse. Remarkably, some of the available vaccine strains show high sequence similarity with local strains in Iraq; however, they are not included in the routine vaccination programs. Analysis of more samples involving more geographical regions is needed to draw a detailed map of antigenic diversity of IBDV in Iraq.
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Abbas, Ali Hadi, Haider Abas AL saegh, and Furkan Sabbar ALaraji. "Sequence diversity and evolution of infectious bursal disease virus in Iraq." F1000Research 10 (September 2, 2021): 293. http://dx.doi.org/10.12688/f1000research.28421.2.
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Background: Infectious Bursal Disease (IBD) is a highly infectious disease which causes huge economic losses to the poultry industry due to the direct impact of the illness and indirect consequences such as decreasing the general immunity of the flock, leaving it naive to other diseases. In Iraq, IBD is highly prevalent despite vaccination programs, yet studies on sequence diversity of the causative virus are still rare. Methods: A sample from Bursa of Fabricius from an IBD outbreak in a flock in the city of Najaf in Iraq was smeared on an FTA card. Amplicons of targeted regions in VP1 and VP2 genes were generated and sequenced. Sequences were then compared with other local and global sequences downloaded from GenBank repositories. Sequence alignment and DNA sequence analyses were achieved using MUSCLE, UGENE and MEGAx software. The molecular clock and sequence evolutionary analyses were applied using MEGAx tools. Results: The strain sequenced in this study belongs to a very virulent Infectious Bursal Disease Virus (vvIBDV) as the DNA and phylogenetic analysis of VP1 and VP2 gene sequences showed a mutual clustering with similar sequences belonging to vvIBDV genogroup 3. Analyses of the hyper variable region of VP2 gene (hvVP2) of IBDV isolates from Iraq indicates a presence of sequence diversity. Interestingly, the two vaccine strains Ventri IBDV Plus and ABIC MB71 that showed the highest sequence similarity to the local isolates in the hvVP2 region are not used in vaccination routine against IBDV in Iraq. Conclusion: Sequences of vvIBDV in Iraq are diverse. Remarkably, some of the available vaccine strains show high sequence similarity with local strains in Iraq; however, they are not included in the routine vaccination programs. Analysis of more samples involving more geographical regions is needed to draw a detailed map of antigenic diversity of IBDV in Iraq.
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Kelemen, Mária, Katalin Forgách, Judit Iván, V. Palya, T. Süveges, B. Tóth, and J. Mészáros. "Pathological and Immunological Study of an in ovo Complex Vaccine against Infectious Bursal Disease." Acta Veterinaria Hungarica 48, no. 4 (December 2000): 443–54. http://dx.doi.org/10.1556/004.48.2000.4.7.
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The appearance of very virulent strains of infectious bursal disease (IBD) virus at the end of the 1980s made it necessary to develop more effective immunization procedures. To facilitate this, the immunogenicity and the immunosuppressive effect of a mild (G-87), an intermediate (LIBD) and an intermediate-plus (IBDV 2512) IBDV strain were tested after the in ovo inoculation of 18-day-old SPF and broiler chicken embryos. It was established that no noteworthy difference existed between the immunized and the control embryos in hatching rate and hatching weight. The higher the virulence of the vaccine virus strain, the more severe damage it caused to the lymphocytes of the bursa of Fabricius. In SPF chickens, the haemagglutination inhibition (HI) titres induced by a Newcastle disease (ND) vaccine administered at day old decreased in inverse ratio to the virulence of the IBD vaccine strain, while in broiler chickens this was not observed. Despite the decrease of the HI titre, the level of protection did not decline, or did so only after the use of the ‘hot’ strain. SPF chickens immunized in ovo with a complex vaccine prepared from strain IBDV 2512 and IBD antibody showed the same protection against Newcastle disease as the broilers. In broiler chicken embryos immunized in ovo, only strain IBDV 2512 induced antibody production, and such chickens were protected against IBD at 3 weeks of age. The complex vaccine administered in ovo has been used successfully at farm hatcheries as well.
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Wang, Yongjuan, Huaichang Sun, Pengpeng Shen, Xinyu Zhang, and Xiaoli Xia. "Effective inhibition of infectious bursal disease virus replication by recombinant avian adeno-associated virus-delivered microRNAs." Journal of General Virology 90, no. 6 (June 1, 2009): 1417–22. http://dx.doi.org/10.1099/vir.0.010520-0.
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RNA interference (RNAi) is a novel antiviral strategy against a variety of virus infections. Infectious bursal disease virus (IBDV) causes an economically important disease in young chickens. This study demonstrated efficient inhibition of IBDV replication by recombinant avian adeno-associated virus (rAAAV)-delivered anti-VP1 and anti-VP2 microRNAs (miRNAs). In the viral vector-transduced cells, sequence-specific miRNA expression was detected by poly(A)-tailed RT-PCR. Reporter assays using a pVP2-EGFP vector showed significant and long-lasting inhibition of VP2–EGFP expression in cells transduced with anti-VP2 miRNA-expressing rAAAV-RFPmiVP2E, but not with the control miRNA-expressing rAAAV-RFPmiVP2con or anti-VP1 miRNA-expressing rAAAV-RFPmiVP1. Semi-quantitative RT-PCR and/or virus titration assays showed a significant inhibitory effect on homologous IBDV replication in cells transduced with rAAAV-RFPmiVP1 or rAAAV-RFPmiVP2E. For two heterologous IBDV isolates, transduction with rAAAV-RFPmiVP1 led to slightly weaker but similar inhibitory effects, whereas transduction with rAAAV-RFPmiVP2E resulted in significantly weaker and different inhibitory effects. These results suggest that rAAAV could act as an efficient vector for miRNA delivery into avian cells and that VP1 is the more suitable target for interfering with IBDV replication using RNAi technology.
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Wang, Yulong, Nan Jiang, Linjin Fan, Li Gao, Kai Li, Yulong Gao, Xinxin Niu, et al. "Development of a Viral-Like Particle Candidate Vaccine Against Novel Variant Infectious Bursal Disease Virus." Vaccines 9, no. 2 (February 10, 2021): 142. http://dx.doi.org/10.3390/vaccines9020142.
Full textAbstract:
Infectious bursal disease (IBD), an immunosuppressive disease of young chickens, is caused by infectious bursal disease virus (IBDV). Novel variant IBDV (nVarIBDV), a virus that can evade immune protection against very virulent IBDV (vvIBDV), is becoming a threat to the poultry industry. Therefore, nVarIBDV-specific vaccine is much needed for nVarIBDV control. In this study, the VP2 protein of SHG19 (a representative strain of nVarIBDV) was successfully expressed using an Escherichia coli expression system and further purified via ammonium sulfate precipitation and size-exclusion chromatography. The purified protein SHG19-VP2-466 could self-assemble into 25-nm virus-like particle (VLP). Subsequently, the immunogenicity and protective effect of the SHG19-VLP vaccine were evaluated using animal experiments, which indicated that the SHG19-VLP vaccine elicited neutralization antibodies and provided 100% protection against the nVarIBDV. Furthermore, the protective efficacy of the SHG19-VLP vaccine against the vvIBDV was evaluated. Although the SHG19-VLP vaccine induced a comparatively lower vvIBDV-specific neutralization antibody titer, it provided good protection against the lethal vvIBDV. In summary, the SHG19-VLP candidate vaccine could provide complete immune protection against the homologous nVarIBDV as well as the heterologous vvIBDV. This study is of significance to the comprehensive prevention and control of the recent atypical IBD epidemic.
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Sachan, Dhama, Latheef, Samad, Mariappan, Munuswamy, Singh, Singh, Malik, and Singh. "Immunomodulatory Potential of Tinospora cordifolia and CpG ODN (TLR21 Agonist) against the Very Virulent, Infectious Bursal Disease Virus in SPF Chicks." Vaccines 7, no. 3 (September 4, 2019): 106. http://dx.doi.org/10.3390/vaccines7030106.
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Infectious bursal disease (IBD), caused by infectious bursal disease virus (IBDV), is characterized by severe immunosuppression in young chicks of 3 to 6 week age group. Although vaccines are available to prevent IBD, outbreaks of disease are still noticed in the field among vaccinated flocks. Further, the birds surviving IBD become susceptible to secondary infections caused by various viral and bacterial agents. This study assessed the immunoprophylactic potential of Cytosine-guanosinedeoxynucleotide (CpG) oligodeoxynucleotides (ODN) and Tinospora cordifolia stem aqueous extract in the specific pathogen free (SPF) chicks, experimentally infected with very virulent IBDV (vvIBDV). Both of these agents (CpG ODN and herbal extract) showed significant increase in the IFN-γ, IL-2, IL-4, and IL-1 levels in the peripheral blood mononuclear cells (PBMCs) (p < 0.05) of chickens in the treatment groups following IBD infection.Further we found significant reduction in mortality rate in vvIBDV infected chicks treated with either, or in combination, compared with the birds of control group. Additionally, the adjuvant or immune enhancing potential of these two immunomodulatory agents with the commercially available IBDV vaccine was determined in chicks. The augmentation of vaccine response in terms of an enhanced antibody titer after vaccination, along with either or a combination of the two agents was noticed. The findings provide a way forward to counter the menace of IBDV in the poultry sector through use of these herbal or synthetic immunomodulatory supplements.
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Mundt, Egbert. "Tissue culture infectivity of different strains of infectious bursal disease virus is determined by distinct amino acids in VP2." Journal of General Virology 80, no. 8 (August 1, 1999): 2067–76. http://dx.doi.org/10.1099/0022-1317-80-8-2067.
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Two types of strains of serotype I of infectious bursal disease virus (IBDV) have been described, on the basis of their ability (IBDV-TC) or inability (IBDV-BU) to infect chicken embryonic cells in culture. However, both types infect B lymphocytes in the bursa of Fabricius of young chickens. To determine the molecular basis for tissue culture infectivity, virus recombinants with chimeric segments A were constructed from IBDV-TC and IBDV-BU by reverse genetics. The region responsible for the different phenotypes was located in VP2. Site-directed mutagenesis identified single amino acids that are responsible for the restriction in infectivity. However, the appropriate amino acid exchanges are strain-specific.
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Ferrero, Diego, Damià Garriga, Aitor Navarro, José F. Rodríguez, and Núria Verdaguer. "Infectious Bursal Disease Virus VP3 Upregulates VP1-Mediated RNA-Dependent RNA Replication." Journal of Virology 89, no. 21 (August 26, 2015): 11165–68. http://dx.doi.org/10.1128/jvi.00218-15.
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Genome replication is a critical step in virus life cycles. Here, we analyzed the role of the infectious bursal disease virus (IBDV) VP3, a major component of IBDV ribonucleoprotein complexes, on the regulation of VP1, the virus-encoded RNA-dependent RNA polymerase (RdRp). Data show that VP3, as well as a peptide mimicking its C-terminal domain, efficiently stimulates the ability of VP1 to replicate synthetic single-stranded RNA templates containing the 3′ untranslated regions (UTRs) from the IBDV genome segments.
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Wong, Raymond Tsz-Yeung, Chung-Chau Hon, Fanya Zeng, and Frederick C. C. Leung. "Screening of differentially expressed transcripts in infectious bursal disease virus-induced apoptotic chicken embryonic fibroblasts by using cDNA microarrays." Journal of General Virology 88, no. 6 (June 1, 2007): 1785–96. http://dx.doi.org/10.1099/vir.0.82619-0.
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Infectious bursal disease virus (IBDV) induces apoptosis and immunosuppression. To understand the molecular mechanisms involved in the pathogenesis of infectious bursal disease (IBD) and the host-directed antiviral responses, cDNA microarrays were used to identify the differentially expressed transcripts in IBDV-infected chicken embryonic fibroblasts. The results suggest a general suppression of surface receptors, including CD40 ligand and SEMA4D. These are related to T- and B-cell activation and differentiation, which may contribute to the immunosuppression of IBD. In addition, activation of genes involved in Toll-like receptor- and interferon (IFN)-mediated antiviral responses was detected. In particular, upregulation of Toll-like receptor 3, a double-stranded (ds) RNA receptor, and MX1, an IFN-inducible antiviral GTPase, may represent the possible host-directed defence responses against the virus and its dsRNA genome. Interestingly, several lines of evidence suggest the modulation of G protein-coupled receptors and receptor tyrosine kinase signalling pathways, especially the possible transactivation of epidermal growth factor receptor by lysophosphatidic acid. Alteration of these may contribute to the previously reported activation of mitogen-activated protein kinases upon IBDV infection, resulting in macrophage activation and inflammatory responses. Additionally, numerous target genes and inducers of nuclear factor kappa B (NF-κB) were upregulated profoundly, implying that IBDV may modulate host-cell survival and apoptosis to support its replication and facilitate viral spread through NF-κB activation. In summary, this investigation of host-gene expression unravelled the candidate physiological pathways involved in host–virus interaction on a molecular level, providing a foundation for researchers to design experiments based on testable hypotheses targeting individual genes.
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Mutinda, W. U., L. W. Njagi, P. N. Nyaga, L. C. Bebora, P. G. Mbuthia, D. Kemboi, J. W. K. Githinji, and A. Muriuki. "Isolation of Infectious Bursal Disease Virus Using Indigenous Chicken Embryos in Kenya." International Scholarly Research Notices 2015 (November 23, 2015): 1–7. http://dx.doi.org/10.1155/2015/464376.
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Infectious bursal disease virus (IBDV) isolates were recovered from outbreaks to initiate activities towards developing a local vaccine strain. Use of indigenous chicken embryos was exploited to determine their potential, promote utilization of local resources for research, and enhance household economic activities. Bursa of Fabricius (BFs) samples from outbreaks shown to be IBDV positive was homogenized and inoculated in 4-week-old specific pathogen-free (SPF) IBDV seronegative white leghorn chicks. The harvested virus was inoculated into 11-day-old indigenous chicken embryos that were IBDV seronegative and passaged serially three times after which they were inoculated into 4-week-old indigenous chicks to test for presence and virulence of propagated virus. Out of 153 BFs collected from outbreaks, 43.8% (67/153) were positive for IBDV antigen and 65.7% (44/67) caused disease in SPF chicks. The embryo mean mortalities were 88% on primary inoculation, 94% in 1st passage, 91% in 2nd passage, and 67% in 3rd passage. After the third passage in embryos all the 44 isolates were virulent in 4-week-old indigenous chicks. The results show that indigenous chicken embryos support growth of IBDV and can be used to propagate the virus as an alternative viral propagating tool for respective vaccine preparation.
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Liu, Meihong, and Vikram N. Vakharia. "Nonstructural Protein of Infectious Bursal Disease Virus Inhibits Apoptosis at the Early Stage of Virus Infection." Journal of Virology 80, no. 7 (April 1, 2006): 3369–77. http://dx.doi.org/10.1128/jvi.80.7.3369-3377.2006.
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ABSTRACT Infectious bursal disease virus (IBDV), the causative agent of a highly contagious disease in chickens, carries a small nonstructural protein (NS). This protein has been implicated to play a role in the induction of apoptosis. In this study, we investigate the kinetics of viral replication during a single round of viral replication and examine the mechanism of IBDV-induced apoptosis. Our results show that it is caspase dependent and activates caspases 3 and 9. Nuclear factor kappa B (NF-κB) is also activated and is required for IBDV-induced apoptosis. The NF-κB inhibitor MG132 completely inhibited IBDV-induced DNA fragmentation, caspase 3 activation, and NF-κB activation. To study the function of the NS protein in this context, we generated the recombinant rGLS virus and an NS knockout mutant, rGLSNSΔ virus, using reverse genetics. Comparisons of the replication kinetics and markers for virally induced apoptosis indicated that the NS knockout mutant virus induces earlier and increased DNA fragmentation, caspase activity, and NF-κB activation. These results suggest that the NS protein has an antiapoptotic function at the early stage of virus infection.
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Simoni, Isabela Cristina, Maria Judite Bittencourt Fernandes, Renata Marconi Custódio, Alda Maria Backx Noronha Madeira, and Clarice Weis Arns. "Susceptibility of cell lines to avian viruses." Revista de Microbiologia 30, no. 4 (December 1999): 373–76. http://dx.doi.org/10.1590/s0001-37141999000400015.
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The susceptibility of the five cell lines - IB-RS-2, RK-13, Vero, BHK-21, CER - to reovirus S1133 and infectious bursal disease virus (IBDV vaccine GBV-8 strain) was studied to better define satisfactory and sensitive cell culture systems. Cultures were compared for presence of CPE, virus titers and detection of viral RNA. CPE and viral RNA were detected in CER and BHK-21 cells after reovirus inoculation and in RK-13 cell line after IBDV inoculation and with high virus titers. Virus replication by production of low virus titers occurred in IB-RS-2 and Vero cells with reovirus and in BHK-21 cell line with IBDV.
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Delgui, Laura, Dolores González, and José F. Rodríguez. "Infectious bursal disease virus persistently infects bursal B-lymphoid DT40 cells." Journal of General Virology 90, no. 5 (May 1, 2009): 1148–52. http://dx.doi.org/10.1099/vir.0.008870-0.
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Infectious bursal disease virus (IBDV), an important avian pathogen, exhibits a specific tropism for immature B-lymphocyte populations. We have investigated the ability of IBDV to replicate in chicken B-lymphoid DT40 cells, a tumour cell line derived from the bursa of Fabricius of a chicken infected with avian leukosis virus. Our results show that IBDV persistently infects DT40 cells. Establishment of the persistent infection is associated with an extensive remodelling of the hypervariable region of the VP2 capsid polypeptide, accumulating 14 amino acid changes during the first 60 days of the persistent infection. The amino acid sequence of the non-structural VP5 polypeptide, involved in virus dissemination, is not altered during the persistent infection. Results described in this report constitute the first demonstration of the ability of IBDV to establish a persistent infection in vitro.
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Wang, Nian, Lizhou Zhang, Yuming Chen, Zhen Lu, Li Gao, Yongqiang Wang, Yulong Gao, et al. "Cyclophilin A Interacts with Viral VP4 and Inhibits the Replication of Infectious Bursal Disease Virus." BioMed Research International 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/719454.
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Nonstructural protein VP4, a serine protease of infectious bursal disease virus (IBDV) that catalyzes the hydrolysis of polyprotein pVP2-VP4-VP3 to form the viral proteins VP2, VP4, and VP3, is essential to the replication of IBDV. However, the interacting partners of VP4 in host cells and the effects of the interaction on the IBDV lifecycle remain incompletely elucidated. In this study, using the yeast two-hybrid system, the putative VP4-interacting partner cyclophilin A (CypA) was obtained from a chicken embryo fibroblast (CEF) expression library. CypA was further confirmed to interact with VP4 of IBDV using co-immunoprecipitation (CO-IP), GST pull-down, and confocal microscopy assays. Moreover, we found that the overexpression of CypA suppressed IBDV replication, whereas the knock-down of CypA by small interfering RNAs promoted the replication of IBDV. Taken together, our findings indicate that the host cell protein CypA interacts with viral VP4 and inhibits the replication of IBDV.
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Yuan, Weifeng, Xinyu Zhang, Xiaoli Xia, and Huaichang Sun. "Inhibition of infectious bursal disease virus infection by artificial microRNAs targeting chicken heat-shock protein 90." Journal of General Virology 93, no. 4 (April 1, 2012): 876–79. http://dx.doi.org/10.1099/vir.0.039172-0.
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Infectious bursal disease virus (IBDV) causes an important disease in young chickens. Chicken heat-shock protein 90 (cHsp90) has been shown to be a functional component of the cellular receptor complex for IBDV infection. This study demonstrates the inhibitory effect of vector-expressed anti-cHsp90α microRNA (miRNA) on IBDV infection. The reporter vectors pcHsp90α-EGFP and pcHsp90β-EGFP were constructed to facilitate effective miRNA selection. Two anti-cHsp90α and one anti-cHsp90β miRNA-expression vectors were constructed for a stable transfection study. Poly(A)-tailed RT-PCR detected sequence-specific miRNA transcription in transfected cells. Semiquantitative RT-PCR showed inhibition of cHsp90 transcription in transfected cells. A virus-titration assay showed that the anti-cHsp90α miRNA, but not the anti-cHsp90β miRNA, had inhibitory effects on IBDV infection. These results suggest that cHsp90α is a functional component of the cellular receptor complex for IBDV infection, and that anti-cHsp90α miRNA could be used as an anti-IBDV reagent.
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Hosseini, S., A. Omar, I. Aini, and A. Ali. "Diagnostic potential of recombinant protein of hexahistidine tag and infectious bursal disease virus VPX expressed in Escherichia coli." Acta Veterinaria Hungarica 55, no. 3 (September 1, 2007): 405–15. http://dx.doi.org/10.1556/avet.55.2007.3.14.
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The current method to detect antibody titre against infectious bursal disease virus (IBDV) in chickens is based on enzyme-linked immunosorbent assay (ELISA) using whole virus as coating antigen. Coating the ELISA plates requires a purified or at least semi-purified preparation of virus as antigen, which needs special skills and techniques. In this study, instead of using whole virus, recombinant protein of hexahistidine tag (His 6 tag) and VPX protein of IBDV expressed in E. coli was used as an alternative antigen to coat the ELISA plates. There was a good correlation coefficient (R 2 = 0.972) between the results of the ELISA using plates coated with monoclonal antibody against His 6 tag and those of the commercial IBDV ELISA kit. Hence, His 6 tag and VPX recombinant protein expressed in E. coli has the potential for the development of ELISA for the measurement of IBDV-specific antibody.
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Akin, A., C. C. Wu, T. L. Lin, and R. W. Keirs. "Chemiluminescent Detection of Infectious Bursal Disease Virus with a PCR-Generated Nonradiolabeled Probe." Journal of Veterinary Diagnostic Investigation 5, no. 2 (April 1993): 166–73. http://dx.doi.org/10.1177/104063879300500205.
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A polymerase chain reaction (PCR)-generated digoxigenin-labeled nonradioactive oligonucleotide probe was developed and utilized in slot-blot hybridization coupled with chemiluminescence for the detection of infectious bursal disease virus (IBDV). The probe was prepared from the RNA of the standard challenge strain (STC) of IBDV serotype 1 by reverse transcription followed by 2 PCR amplifications with 2 separate sets of primers. RNA of STC viruses prepared from bursae infected with STC viruses was subjected to the first PCR with the outer primers V8 and V9 that amplified a 607-base pair (bp) segment. The PCR product from the first PCR was eluted following agarose gel electrophoresis and subjected to the second PCR with the nested primers V6 and V7 that flanked a 351-bp segment. In the second PCR, dTTP was substituted by digoxigenin-11-dUTP in the PCR reaction mixture so that the amplified 351-bp DNA products were labeled with digoxigenin. The specificity of the PCR-generated digoxigenin-labeled probe was tested on different strains of IBDV, several unrelated avian viruses, and bacteria by slot-blot hybridization assay. Hybridization was detected by chemiluminescence. The sensitivity of the probe was assayed using lo-fold serial dilutions of purified RNA from the STC strain of IBDV. The PCR-generated digoxigenin-labeled probe hybridized with genomic RNA of STC and variant strains A, D, E, G, and GLS-5 of IBDV serotype 1 but not OH strain of IBDV serotype 2. The probe did not react with avian reovirus, infectious bronchitis virus, Salmonella enteritidis, Escherichia coli, or Staphylococcus aureus. The probe was very sensitive, and as little as 72 fg of RNA from the STC strain of IBDV could be detected. The results indicate that this PCR-generated digoxigenin-labeled nonisotopic probe is specific for IBDV and may be utilized in a diagnostic assay for all IBDV serotype 1 strains.
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Pikuła, Anna, Katarzyna Domańska-Blicharz, Rytis Cepulis, and Krzysztof Śmietanka. "Identification of infectious bursal disease virus with atypical VP2 amino acid profile in Latvia." Journal of Veterinary Research 61, no. 2 (June 1, 2017): 145–49. http://dx.doi.org/10.1515/jvetres-2017-0018.
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AbstractIntroduction: Infectious bursal disease virus (IBDV) is a causative agent of immunosuppressive disorder resulting in significant losses to the world poultry industry. This study describes the molecular characterisation of an atypical IBDV from a field outbreak that occurred in vaccinated chicken flocks in Latvia in 2011.Material and Methods: Ten bursae of Fabricius from each flock were collected for laboratory examination. Virus isolation was performed in embryonated eggs and CEF culture. The RT-PCR aimed at hypervariable domain of VP2 gene combined with sequencing was performed for detection and identification of IBDV.Results: The molecular examinations confirmed the IBDV infection. The analysis of the amino acid sequence revealed that the strain possessed four amino acids at VP2 protein (222A, 256I, 294I, and 299S), indicating a genetic relatedness to a very virulent IBDV. However, some unique or rare amino acid substitutions (219L, 220F, 254D, 279N, and 280T) were also detected.Conclusion: The obtained results demonstrate the occurrence of IBDV with a high mutation rate within the hypervariable domain of VP2 peptide, and highlight the necessity of implementation of IBDV surveillance in Eastern European poultry industry to determine whether this strain is an exception or a new wave of IBDV with new genetic features emerged in the field.
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Boot, Hein J., A. Agnes H. M. ter Huurne, Arjan J. W. Hoekman, Jan M. Pol, Arno L. J. Gielkens, and Ben P. H. Peeters. "Exchange of the C-Terminal Part of VP3 from Very Virulent Infectious Bursal Disease Virus Results in an Attenuated Virus with a Unique Antigenic Structure." Journal of Virology 76, no. 20 (October 15, 2002): 10346–55. http://dx.doi.org/10.1128/jvi.76.20.10346-10355.2002.
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ABSTRACT Infectious bursal disease virus (IBDV) is the major viral pathogen in the poultry industry. Live attenuated serotype 1 vaccine strains are commonly used to protect susceptible chickens during their first 6 weeks of life. Wild-type serotype 1 IBDV strains are highly pathogenic only in chickens, whereas serotype 2 strains are apathogenic in chickens and other birds. Here we describe the replacement of the genomic double-stranded RNA (dsRNA) encoding the N- or C-terminal part of VP3 of serotype 1 very virulent IBDV (vvIBDV) (isolate D6948) with the corresponding part of serotype 2 (isolate TY89) genomic dsRNA. The modified virus containing the C-terminal part of serotype 2 VP3 significantly reduced the virulence in specific-pathogen-free chickens, without affecting the distinct bursa tropism of serotype 1 IBDV strains. Furthermore, by using serotype-specific antibodies we were able to distinguish bursas infected with wild-type vvIBDV from bursas infected with the modified vvIBDV. We are currently evaluating the potential of this recombinant strain as an attenuated live vaccine that induces a unique serological response (i.e., an IBDV marker vaccine).
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Jungmann, Annett, Hermann Nieper, and Hermann Müller. "Apoptosis is induced by infectious bursal disease virus replication in productively infected cells as well as in antigen-negative cells in their vicinity." Journal of General Virology 82, no. 5 (May 1, 2001): 1107–15. http://dx.doi.org/10.1099/0022-1317-82-5-1107.
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The kinetics of infectious bursal disease virus (IBDV) replication and induction of apoptosis were investigated in vitro and in vivo. After infection of chicken embryo (CE) cells with IBDV strain Cu-1, the proportion of apoptotic cells increased from 5·8% at 4 h post-infection (p.i.) to 64·5% at 48 h p.i. The proportion of apoptotic cells correlated with IBDV replication. UV-inactivated IBDV particles did not induce apoptosis. Double labelling revealed that, early after infection, the majority of antigen-expressing cells were not apoptotic; double-labelled cells appeared more frequently at later times. Remarkably, apoptotic cells were frequently located in the vicinity of antigen-expressing cells. This indicated that an apoptosis-inducing factor(s) might be released by cells that replicate IBDV. Since interferon (IFN) production has been demonstrated after IBDV infection, IFN was considered to be one of several factors. However, supernatants of infected CE cells in which virus infectivity had been neutralized were not sufficient to induce apoptosis.Similar results were observed in the infected bursae of Fabricius: early after infection, most of the cells either showed virus antigens or were apoptotic. Again, double-labelled cells appeared more frequently late after infection. This suggests that indirect mechanisms might also be involved in the induction of apoptosis in vivo, contributing to the rapid depletion of cells in the IBDV-infected bursa.
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Lin, Ta-Wei, Chi-Wen Lo, Su-Yuan Lai, Ruey-Jane Fan, Chao-Jung Lo, Yu-mei Chou, Rekha Thiruvengadam, Andrew H. J. Wang, and Min-Ying Wang. "Chicken Heat Shock Protein 90 Is a Component of the Putative Cellular Receptor Complex of Infectious Bursal Disease Virus." Journal of Virology 81, no. 16 (May 23, 2007): 8730–41. http://dx.doi.org/10.1128/jvi.00332-07.
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ABSTRACT Infectious bursal disease virus (IBDV) causes a highly contagious disease in young chicks and leads to significant economic losses in the poultry industry. The capsid protein VP2 of IBDV plays an important role in virus binding and cell recognition. VP2 forms a subviral particle (SVP) with immunogenicity similar to that of the IBDV capsid. In the present study, we first showed that SVP could inhibit IBDV infection to an IBDV-susceptible cell line, DF-1 cells, in a dose-dependent manner. Second, the localizations of the SVP on the surface of DF-1 cells were confirmed by fluorescence microscopy, and the specific binding of the SVP to DF-1 cells occurred in a dose-dependent manner. Furthermore, the attachment of SVP to DF-1 cells was inhibited by an SVP-induced neutralizing monoclonal antibody against IBDV but not by denatured-VP2-induced polyclonal antibodies. Third, the cellular factors in DF-1 cells involved in the attachment of SVP were purified by affinity chromatography using SVP bound on the immobilized Ni2+ ions. A dominant factor was identified as being chicken heat shock protein 90 (Hsp90) (cHsp90) by mass spectrometry. Results of biotinylation experiments and indirect fluorescence assays indicated that cHsp90 is located on the surface of DF-1 cells. Virus overlay protein binding assays and far-Western assays also concluded that cHsp90 interacts with IBDV and SVP, respectively. Finally, both Hsp90 and anti-Hsp90 can inhibit the infection of DF-1 cells by IBDV. Taken together, for the first time, our results suggest that cHsp90 is part of the putative cellular receptor complex essential for IBDV entry into DF-1 cells.
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von Einem, Ursula I., Alexander E. Gorbalenya, Horst Schirrmeier, Sven-Erik Behrens, Tobias Letzel, and Egbert Mundt. "VP1 of infectious bursal disease virus is an RNA-dependent RNA polymerase." Journal of General Virology 85, no. 8 (August 1, 2004): 2221–29. http://dx.doi.org/10.1099/vir.0.19772-0.
Full textAbstract:
Segment B of the bisegmented, double-stranded RNA genome of infectious bursal disease virus (IBDV) encodes the viral protein VP1. This has been presumed to represent the RNA-dependent RNA polymerase (RdRp) as it contains motifs that are typical for the RdRp of plus-strand RNA viruses. Here it is demonstrated that baculovirus-expressed wild-type but not motif A mutated VP1 acts as an RdRp on IBDV-specific RNA templates. Thus, on a plus-strand IBDV segment A cRNA template, minus-strand synthesis occurred in such a way that a covalently linked double-stranded RNA product was generated (by a ‘copy-back’ mechanism). Importantly, enzyme activity was observed only with templates that comprised the 3′ non-coding region of plus-strand RNAs transcribed from IBDV segments A and B, indicating template specificity. RdRp activity was shown to have a temperature optimum of 37 °C and required magnesium ions for enzyme activity. Thus, it has been demonstrated unequivocally that VP1 represents the RdRp of IBDV.
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Wang, Suyan, Mengmeng Yu, Aijing Liu, Yuanling Bao, Xiaole Qi, Li Gao, Yuntong Chen, et al. "TRIM25 inhibits infectious bursal disease virus replication by targeting VP3 for ubiquitination and degradation." PLOS Pathogens 17, no. 9 (September 13, 2021): e1009900. http://dx.doi.org/10.1371/journal.ppat.1009900.
Full textAbstract:
Infectious bursal disease virus (IBDV), a double-stranded RNA virus, causes immunosuppression and high mortality in 3–6-week-old chickens. Innate immune defense is a physical barrier to restrict viral replication. After viral infection, the host shows crucial defense responses, such as stimulation of antiviral effectors to restrict viral replication. Here, we conducted RNA-seq in avian cells infected by IBDV and identified TRIM25 as a host restriction factor. Specifically, TRIM25 deficiency dramatically increased viral yields, whereas overexpression of TRIM25 significantly inhibited IBDV replication. Immunoprecipitation assays indicated that TRIM25 only interacted with VP3 among all viral proteins, mediating its K27-linked polyubiquitination and subsequent proteasomal degradation. Moreover, the Lys854 residue of VP3 was identified as the key target site for the ubiquitination catalyzed by TRIM25. The ubiquitination site destroyed enhanced the replication ability of IBDV in vitro and in vivo. These findings demonstrated that TRIM25 inhibited IBDV replication by specifically ubiquitinating and degrading the structural protein VP3.
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Parapatla, Harshavardhan Reddy, Kiran Kumar J, Sunil Kumar Myla, and Charitha Devi Mekala. "Isolation and characterization of Infectious bursal disease virus VP2 gene isolated from Tirupati region of Andhra Pradesh, India." Journal of Applied Virology 5, no. 4 (May 2, 2017): 79. http://dx.doi.org/10.21092/jav.v5i4.79.
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<p>Infectious bursal disease (IBD) is a highly contagious viral disease of birds characterized by lesions in the bursa of Fabricius, immunosuppression, severe morbidity and mortality. Due to amino acids substitutions in this region results in change in the topography of hyper variable region of VP2, where most of the neutralizing epitopes are present. Cloning and characterization of hyper variable region of prevalent strains of IBDV in this part of the country will provide basis for development of better vaccine for future. In the present study, we cloned four full length sequences of IBDV-VP2 with hyper variable region and found that all the cloned sequences have similar epitopes. Phylogenetic analysis showed that they are closely related to each other and are also closely related to strains of Luxembourg, China, and USA. This study will enhance the knowledge on IBDV circulating strains in this part of the country.</p>
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Oluwayelu, Daniel Oladimeji, Adebowale Idris Adebiyi, Ibukunoluwa Olaniyan, Phyllis Ezewele, and Oluwasanmi Aina. "Occurrence of Newcastle Disease and Infectious Bursal Disease Virus Antibodies in Double-Spurred Francolins in Nigeria." Journal of Veterinary Medicine 2014 (November 18, 2014): 1–5. http://dx.doi.org/10.1155/2014/106898.
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The double-spurred francolin Francolinus bicalcaratus has been identified as a good candidate for future domestication due to the universal acceptability of its meat and its adaptability to anthropogenically altered environments. Therefore, in investigating the diseases to which they are susceptible, serum samples from 56 francolins in a major live-bird market (LBM) in Ibadan, southwestern Nigeria, were screened for antibodies against Newcastle disease (ND) and infectious bursal disease (IBD) viruses. Haemagglutination inhibition (HI) test and enzyme-linked immunosorbent assay (ELISA) revealed 25.0% and 35.7% prevalence of ND virus (NDV) antibodies, respectively, while 5.4% and 57.1% prevalence of IBD virus (IBDV) antibodies was detected by agar gel precipitation test (AGPT) and ELISA, respectively. This first report on the occurrence of NDV and IBDV antibodies in apparently healthy, unvaccinated double-spurred francolins from a LBM suggests that they were subclinically infected with either field or vaccine viruses and could thus serve as possible reservoirs of these viruses to domestic poultry. Furthermore, if they are to be domesticated for intensive rearing, a vaccination plan including ND and IBD should be developed and implemented.
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Li, Long, Yao-Wei Huang, Lian-Sheng Wang, Wang-Jun Wan, and Lian Yu. "Synthesis of Reassortant Infectious Bursal Disease Virus in Chickens Injected Directly with Infectious Clones from Different Virus Strains." Acta Biochimica et Biophysica Sinica 37, no. 3 (March 1, 2005): 192–98. http://dx.doi.org/10.1093/abbs/37.3.192.
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Abstract The infectious bursal disease virus (IBDV), a member of the Birnaviridae family, containing a bisegmented double-stranded RNA genome, encodes four structural viral proteins, VP1, VP2, VP3, and VP4, as well as a non-structural protein, VP5. In the present paper, the segment A from two IBDV strains, field isolate ZJ2000 and attenuated strain HZ2, were inserted into one NaeI site by site-directed silent mutagenesis and subcloned into the eukaryotic expression plasmid pCI under the control of the human cytomegalovirus (hCMV) immediate early enhancer and promoter to construct the recombinant plasmids pCI-AKZJ2000 and pCI-AKHZ2, respectively. Each of the two recombinants was combined with another recombinant pCI plasmid containing the marked segment B of strain HZ2 (pCI-mB), and injected intramuscularly into nonimmunized chickens. Two chimeric IBDV strains were recovered from the chickens. Two out of eight chickens in each of two groups showed the bursal histopathological change. The reassortant virus derived from pCI-AKZJ2000/pCI-mB can infect chicken embryos and shows relatively low virulence. We have developed a novel virus reverse genetic approach for the study of IBDV. The results also form the basis for investigating the role of VP1 in viral replication and pathogenecity.
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Yao, Kun, Mark A. Goodwin, and Vikram N. Vakharia. "Generation of a Mutant Infectious Bursal Disease Virus That Does Not Cause Bursal Lesions." Journal of Virology 72, no. 4 (April 1, 1998): 2647–54. http://dx.doi.org/10.1128/jvi.72.4.2647-2654.1998.
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ABSTRACT A reverse genetics system for birnavirus, based on synthetic transcripts of the infectious bursal disease virus (IBDV) genome, was recently developed (E. Mundt and V. N. Vakharia, Proc. Natl. Acad. Sci. USA 93:11131–11136, 1996). To study the function of the 17-kDa nonstructural (NS) protein in viral growth and pathogenesis, we constructed a cDNA clone of IBDV segment A in which the first and only initiation codon (ATG) of NS protein was mutated to a stop codon (TAG). Transfection of Vero cells with combined transcripts of either modified or unmodified segment A, and with segment B, generated viable IBDV progeny. When chicken embryo fibroblast cells infected with transfectant viruses were analyzed by immunofluorescence assays using NS-specific antiserum, the mutant virus did not yield a fluorescence signal, indicating a lack of NS protein expression. Furthermore, replication kinetics and cytotoxic effects of the mutant virus were compared with those of the parental attenuated vaccine strain of IBDV (D78) in vitro. The mutant virus grew to slightly lower titers than D78 virus and exhibited decreased cytotoxic and apoptotic effects in cell culture. To evaluate the characteristics of the recovered viruses in vivo, we inoculated 3-week-old chickens with D78 or mutant virus and analyzed their bursa for histopathological lesions. The recovered D78 virus caused microscopic lesions and atrophy of the bursa, while the mutant virus failed to induce any pathological lesions or clinical signs of disease. In both instances, the virus was recovered from the bursa, and the presence or absence of mutation in these viruses was confirmed by nucleotide sequence analysis of NS gene. Although the mutant virus exhibited a delay in replication in vivo, it induced levels of IBDV neutralizing antibodies that were similar to those of D78 virus. In addition, no reversion of mutation was detected in the mutant virus recovered from inoculated chickens. These results demonstrate that NS protein is dispensable for viral replication in vitro and in vivo and that it plays an important role in viral pathogenesis. Thus, generation of such NS protein-deficient virus will facilitate the study of immunosuppression and aid in the development of live-attenuated vaccines for IBDV.
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Hollmén, Tuula, J. Christian Franson, Douglas E. Docherty, Mikael Kilpi, Martti Hario, Lynn H. Creekmore, and Margaret R. Petersen. "Infectious Bursal Disease Virus Antibodies in Eider Ducks and Herring Gulls." Condor 102, no. 3 (August 1, 2000): 688–91. http://dx.doi.org/10.1093/condor/102.3.688.
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Abstract We measured antibodies to infectious bursal disease virus (IBDV) in blood of nesting Common Eider (Somateria mollissima) females and immature Herring Gulls (Larus argentatus) in the Baltic Sea, and in blood of Spectacled Eider (Somateria fischeri) females nesting in a remote area of western Alaska. Positive (≥ 1:16) IBDV titers occurred in 75% of the eiders and 45% of the Herring Gull chicks. In eiders, the prevalence of positive titers differed among locations. We found no evidence that IBDV exposure impaired the immune function of Herring Gull chicks, based on their response to inoculation of sheep red blood cells. We suggest that eider ducks and Herring Gulls have been exposed to IBDV, even in locations where contact with poultry is unlikely. The presence of this virus in wild bird populations is of concern because it causes mortality of up to 30% in susceptible poultry.
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Huo, Shanshan, Jianlou Zhang, Jinghui Fan, Xing Wang, Fengyang Wu, Yuzhu Zuo, and Fei Zhong. "Co-Expression of Chicken IL-2 and IL-7 Enhances the Immunogenicity and Protective Efficacy of a VP2-Expressing DNA Vaccine against IBDV in Chickens." Viruses 11, no. 5 (May 24, 2019): 476. http://dx.doi.org/10.3390/v11050476.
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Chicken infectious bursal disease (IBD) is still incompletely controlled worldwide. Although IBD virus (IBDV) VP2 DNA vaccine was considered a safe vaccine for IBD prevention, the immunogenicity by itself remains poor, resulting in the failure of effectively protecting chickens from infection. We and others demonstrated that chicken IL-2 (chIL-2) and chIL-7 have the capacity to enhance the immunogenicity of the VP2 DNA vaccine. However, whether chIL-2 and chIL-7 can mutually enhance the immunogenicity of VP2 DNA vaccine and thereby augment the latter’s protection efficacy remains unknown. By using chIL-2/chIL-7 bicistronic gene vector to co-immunize the chickens together with the VP2 DNA vaccine, we now show that chIL-2 and chIL-7 significantly increased IBDV VP2-specific antibody titers, T cell proliferation, and IFN-γ production, resulting in the ultimate enhancement of vaccine-induced protection efficacy relative to that of chIL-2 or chIL-7 gene vectors alone. These results suggest that chIL-2 and chIL-7 can mutually enhance VP2 DNA vaccine’s efficacy, thereby establishing a concrete foundation for future optimization of IBDV VP2 DNA vaccine to prevent/treat chicken IBD.
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Meng, Yufang, Xiaoxue Yu, Chunxue You, Wenjuan Zhang, Yingfeng Sun, Liuan Li, Tianming Jin, Pengyu Pan, and Ailing Xie. "Chicken Heat Shock Protein 70 Is an Essential Host Protein for Infectious Bursal Disease Virus Infection In Vitro." Pathogens 10, no. 6 (May 28, 2021): 664. http://dx.doi.org/10.3390/pathogens10060664.
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Infectious bursal disease virus (IBDV) infection causes pathogenicity and mortality in chickens, leading to huge economic losses in the poultry industry worldwide. Studies of host-virus interaction can help us to better understand the viral pathogenicity. As a highly conservative host factor, heat shock protein 70 (Hsp70) is observed to be involved in numerous viral infections. However, there is little information about the role of chicken Hsp70 (cHsp70) in IBDV infection. In the present study, the increased expression of cHsp70 was observed during IBDV-infected DF-1 cells. Further studies revealed that Hsp70 had similar locations with the viral double-stranded RNA (dsRNA), and the result of pull-down assay showed the direct interaction between cHsp70 with dsRNA, viral proteins (vp)2 and 3, indicating that maybe cHsp70 participates in the formation of the replication and transcription complex. Furthermore, overexpression of cHsp70 promoted IBDV production and knockdown of cHsp70 using small interfering RNAs (siRNA) and reducedviral production, implying the necessity of cHsp70 in IBDV infection. These results reveal that cHsp70 is essential for IBDV infection in DF-1 cells, suggesting that targeting cHsp70 may be applied as an antiviral strategy.
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Gethöffer, Friederike, Nele Curland, Ulrich Voigt, Benno Woelfing, Tobias Ludwig, Ursula Heffels-Redmann, Hafez Mohamed Hafez, Michael Lierz, and Ursula Siebert. "Seroprevalences of specific antibodies against avian pathogens in free-ranging ring-necked pheasants (Phasianus colchicus) in Northwestern Germany." PLOS ONE 16, no. 8 (August 4, 2021): e0255434. http://dx.doi.org/10.1371/journal.pone.0255434.
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Infectious diseases in captive pheasants (Phasianus colchicus) are well known, but there is a lack of knowledge about occurrence and distribution of pathogens in free-ranging pheasants in Germany. We investigated 604 sera from hunted pheasants and 152 sera from wild caught pheasants between 2011 to 2015, with the aim to determine the prevalence of specific antibodies against different viruses: Avian influenza virus (AIV) of subtypes H5, H7, H9, paramyxovirus type 1 (PMV-1), avian encephalomyelitis virus (AEV), infectious bursitis disease virus (IBDV), infectious bronchitis virus (IBV), infectious laryngotracheitis virus (ILTV), avian metapneumovirus (aMPV) and Salmonella sp., Mycoplasma synoviae (MS) and Mycoplasma gallisepticum (MG). In addition, 178 caeca were investigated for Histomonas meleagridis. The study reveals an ongoing circulation of IBV in the wild pheasant population during the study. Also high seroprevalences of specific antibodies against aMPV depending on the area and a strong increase in prevalence of IBDV antibodies in sera of pheasants in Lower Saxony were detected. ILTV antibody prevalences differed between areas and AEV antibody detection differed between years significantly, whereas specific antibodies against PMV-1 could not be detected and antibodies against AIV-H5, -H7 and -H9 and Mycoplasma spp. were detected in very few cases.
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Stoute, Simone T., Daral J. Jackwood, Beate M. Crossley, Linda O. Michel, and Julia R. Blakey. "Molecular epidemiology of endemic and very virulent infectious bursal disease virus genogroups in backyard chickens in California, 2009–2017." Journal of Veterinary Diagnostic Investigation 31, no. 3 (April 4, 2019): 371–77. http://dx.doi.org/10.1177/1040638719842193.
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Pathogenic strains of infectious bursal disease virus (IBDV) are associated with increased morbidity, mortality, and immunosuppression in susceptible chickens. Backyard poultry is increasing in popularity in the United States, but very little is known about the prevalence and molecular epidemiology of IBDV within these flocks. We performed a retrospective study and phylogenetic analyses of IBDV detected in backyard chickens (BYCs) submitted to the California Animal Health and Food Safety (CAHFS) diagnostic laboratory system in 2009–2017. There were 17 CAHFS autopsy cases of very virulent IBDV (vvIBDV) segment A detected by RT-rtPCR in BYC flocks from 7 counties in California from 2009–2017. During this same time period, non-vvIBDV genotypes were detected by RT-rtPCR in 16 autopsy cases originating from BYC premises in 10 counties in California. Subsequent RT-PCR and phylogenetic analysis of a segment of the hvVP2 and VP1 gene identified vvIBDV, interserotypic reassortant IBDV (vvIBDV segment A and serotype 2 segment B), and non-vvIBDV (variant/subclinical IBDV and classic IBDV) strains in BYC flocks in California.
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Naggar, Rania F. El, Mohammed A. Rohaim, and Muhammad Munir. "Potential reverse spillover of infectious bursal disease virus at the interface of commercial poultry and wild birds." Virus Genes 56, no. 6 (September 24, 2020): 705–11. http://dx.doi.org/10.1007/s11262-020-01793-x.
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AbstractRecently, multiple spillover events between domesticated poultry and wild birds have been reported for several avian viruses. This phenomenon highlights the importance of the livestock-wildlife interface in the possible emergence of novel viruses. The aim of the current study was to investigate the potential spillover and epidemiological links of infectious bursal disease virus (IBDV) between wild birds and domestic poultry. To this end, twenty-eight cloacal swabs were collected from four species of free-living Egyptian wild birds (i.e. mallard duck, bean goose, white-fronted goose and black-billed magpie). Genetic and phylogenetic analysis of three positive isolates revealed that the IBDV/USC-1/2019 strain clustered with previously reported very virulent IBDV (vvIBDV) Egyptian isolates. Interestingly, two other wild bird-origin isolates (i.e. IBDV/USC-2/2019 and IBDV/USC-3/2019) grouped with a vaccine strain that is being used in commercial poultry. In conclusion, our results revealed the molecular detection of vaccine and vvIBDV-like strains in Egyptian wild birds and highlighted the potential role of wild birds in IBDV epidemiology in disease-endemic regions.
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Noor, M., C. Lüken, PM Das, MR Islam, and H. Müller. "Regeneration of a recombinant infectious bursal disease virus having four amino acid substitutions in VP2 by reverse genetics." Bangladesh Veterinarian 31, no. 1 (March 31, 2015): 12–19. http://dx.doi.org/10.3329/bvet.v31i1.22838.
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Infectious bursal disease virus (IBDV), a virus with a double-stranded, bi-segmented RNA genome, is an economically important pathogen of chickens. Recent understanding of the molecular biology of IBDV has implicated several amino acid residues in the capsid protein VP2 in pathogenicity and tissue culture adaptation. In the present study a recombinant strain of IBDV having four mutations in VP2 (Gln253His, Asp279Asn, Ala284Thr and Ser330Arg) has been generated using reverse genetics. Desired mutations were introduced in the VP2 gene of the cloned cDNA of genome segment A of a very virulent (vv) IBDV by site-directed mutagenesis. Capped RNA transcribed in vitro from cloned cDNA of the modified segment A and wild type segment B was co-transfected into chicken embryo fibroblast (CEF) cell culture. The recombinant virus, designated as BD- 3tcC, was rescued from the transfected cell culture and characterized in vitro. BD-3tcC retained all the four desired mutations and replicated with titres only slightly lower than those of CEF cell-culture-adapted wild-type IBDV. This recombinant strain can be used in future studies for understanding the biological significance of these four amino acid residues in VP2. DOI: http://dx.doi.org/10.3329/bvet.v31i1.22838 Bangl. vet. 2014. Vol. 31, No. 1, 12-19