SEARCH · PubMed Health

Results for “IBDV”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 343 records · Page 19Linked to original sources

PubMed1979

Morphologic changes in the bursa of fabricius of chickens after inoculation with infectious bursal disease virus.

Sequential morphologic changes in the bursa of Fabricius were studied after oral inoculation of 1-day-old chicks with infectious bursal disease virus (IBDV). The epithelial surface morphology was studied by scanning electron microscopy, whereas the IBDV replication was sequentially followed by immunofluorescence and transmission electron microscopy. The earliest detectable changes in the bursal epithelium were evident at postinoculation hour (PIH) 48. They were characterized by reduction in numbers and size of microvilli on the epithelial cells accompanied by gradual involution of the button-like bursal follicles. At PIH 96 some specimens showed localized surface erosions due to loss of epithelial cells. As the damage progressed, the infolding of the buttomlike follicles became more pronounced and the surface erosions became more extensive. Loss of surface epithelium exposed the underlying damaged bursal follicles which appeared to be bounded by columnar epithelium. Some follicles had lost almost all the lymphocytes and macrophages and appeared as empty craters. Intrafollicular replication of IBDV was detectable as early as PIH 24 by immunofluorescence technique. Viral replication primarily took place in the lymphoid follicles. Regeneration of the follicles was not seen up to postinoculation day 12, suggesting that the IBDV-induced bursal damage could be permanent.

Animals↗

PubMed1986

Effect of attenuated viral vaccines on suckling mice infected with LCMV.

A single intraperitoneal treatment with live Newcastle Disease Virus (NDV) containing attenuated NDV vaccine, and with live infectious bursal disease virus (IBDV) containing attenuated IBDV vaccine, one day before intracerebral infection with lymphocytic choriomeningitis virus (LCMV) increased, whereas a similar treatment with inactivated NDV or IBDV vaccine did not influence the death rate of suckling mice from experimental lymphocytic choriomeningitis. Thus the attenuated live vaccine stimulated, whereas the inactivated ones failed to affect the cell-mediated immune response to LCMV. Control studies set up with the supernatant of plain tissue culture routinely used for the propagation of IBDV have shown that unlike the attenuated NDV vaccine, the immunostimulatory action is associated not so much with the virus itself, as with an as yet unidentified component of the tissue culture supernatant.

Animals↗

PubMedDate not supplied

Effects of chemically or virus-induced immunodepression on response of chickens to avian leukosis virus.

The effects of chemically or virus-induced immunodepression on the infection profile (development of viremia and antibody) and shedding of avian leukosis virus (ALV) were studied in progeny chickens of experimental or commercial breeder flocks. Chickens were infected with ALV subgroup A by contact at hatching and by oral inoculation at 4-5 weeks of age. In the first experiment, chickens were inoculated with a virulent strain of infectious bursal disease virus (IBDV) at 1 day or 6 weeks of age. In the second experiment, chickens were neonatally treated with cyclophosphamide (CY), or were inoculated with strain T of reticuloendotheliosis virus (REV) at hatching, or were inoculated with strain JM of Marek's disease virus (MDV) at 2 weeks of age. The infection profile and cloacal shedding of ALV in chickens exposed to ALV and inoculated with immunodepressive viruses or CY were compared with those in hatchmates exposed only to ALV. In two of four chicken lines tested in the first experiment, shedding of ALV, as determined by virological assays of cloacal swabs at 22 weeks of age, was significantly higher in chickens infected with IBDV at 1 day of age than in uninfected hatchmates. The rate of shedding of ALV in one of these two lines was also significantly higher in chickens infected with IBDV at 6 weeks of age than in uninfected chickens. Further, the frequency of ALV-antibody detection at 22 weeks of age was significantly lower in chickens of these two lines infected with IBDV at 1 day of age than in uninfected chickens. In the second experiment, neonatal treatment with CY significantly increased the frequency of viremic chickens of both experimental and commercial flocks. The frequency of ALV-viremic chickens at 22 weeks of age was considerably higher in the REV- and MDV-inoculated groups (54% and 44%, respectively) than in control hatchmates (29%), but only in chickens of the commercial line. These findings suggest that chemically or virus-induced immunodepression may lead to an increase in rates of viremia and shedding of ALV in chickens infected with virus after hatching, especially in certain genetic lines.

Animals↗

PubMedDate not supplied

Effect of avian reoviruses on lymphoid organ weights and antibody response in chickens.

Several avian reoviruses were screened to determine their effects on the immune system by inoculating them subcutaneously (SQ) into day-old chicks. For comparison, infectious bursal disease virus (IBDV) was similarly evaluated. The response of the immune system was measured functionally by the hemagglutination-inhibition (HI) response to Newcastle disease virus (NDV) and structurally by changes in the organ-to-body-weight ratios of the bursa of Fabricius, thymus, and spleen. When inoculated SQ, most of the reoviruses caused transient alterations in lymphoid organ weights, decreasing the bursa weight and increasing the spleen weight. Of those reoviruses tested, only one--a commercial vaccine based on the isolate S-1133--demonstrated the ability to interfere significantly with NDV-HI responses, although several had numerically lower titers. Two of the isolates were also evaluated by oral inoculation. Giving the viruses orally did not cause any alterations in organ weights; however, both isolates depressed the HI response of chicks to NDV. Compared with reoviruses, IBDV significantly depressed NDV-HI titers. The structural responses to IBDV differed, however: IBDV significantly depressed bursa weights for all 3 weeks of the test period without affecting spleen weights. Some of the reovirus isolates inoculated SQ were lethal for day-old chicks. This, and their ability to alter the lymphoid-to-body-weight ratios of the spleen and bursa, could be considered valid criteria by which to study the pathogenesis of these agents.

Animals↗

PubMedDate not supplied

Pathology of avian adenovirus serotypes in the presence of Escherichia coli in infectious-bursal-disease-virus-infected specific-pathogen-free chickens.

Ten strains of adenovirus representing 10 serotypes were administered intratracheally to 3-week-old specific-pathogen-free chickens, which also received 2.5 X 10(5) colony-forming units of a pathogenic Escherichia coli intranasally. Those birds had been inoculated by eye drop at 1 day of age with a virulent infectious bursal disease virus (IBDV). Controls consisted of groups of chickens inoculated with: (a) IBDV and E. coli, (b) IBDV only, (c) E. coli only, and (d) no virus or E. coli. Gross pulmonary alterations at 5 days postinoculation (PI) included congestion and consolidation of one or both lungs of a chick inoculated with adenovirus serotype Ind-C and another inoculated with A-2. Histopathologic alterations in the lungs were those of multifocal interstitial and occasionally diffuse pneumonia. All 10 adenovirus serotypes elicited multifocal or diffuse pneumonia and bronchiolitis in one or more of the five birds per group necropsied at 5 days PI. T-8 and A-2 serotypes induced marked to serve diffuse pneumonia within 5 days; Ind-C, Stein, Tipton, 75-1A, B-3, and X-11 incited a mild diffuse pneumonia. In all groups, the pneumonic lesions were more severe 5 days PI than 12 days PI. Tracheitis was incited by Ind-C, Stein, T-8, and A-2 at 5 days PI; the lesions were minimal to marked in severity. None of the four control groups exhibited gross or histopathologic alterations except the two IBDV-infected groups, which exhibited bursal change.

Adenoviridae Infections↗

PubMedDate not supplied

A comparison between the effect of an avian reovirus and infectious bursal disease virus on selected aspects of the immune system of the chicken.

Reovirus 81-176 was inoculated subcutaneously into day-old specific-pathogen-free leghorns and evaluated for its effects on the immune system over a 3-week period. Structural criteria included organ weights of the bursa of Fabricius (BF) and spleen (SP), scoring of histological lesions in the BF, SP, and thymus, and hematological analyses of the circulating leukocytes. Alterations in the functional capacity of the immune system were measured using the graft-versus-host reaction, the response of peripheral blood lymphocytes (PBLs) to mitogens, the ability of circulating monocytes to phagocytize latex beads, and the serological responses to Newcastle disease virus, sheep red blood cells, and Brucella abortus antigens. For comparison, infectious bursal disease virus (IBDV) was similarly evaluated by most of the same tests. Structurally, reovirus 81-176 altered BF and SP organ weights, the total numbers of white blood cells in circulation, and the degree of follicular atrophy in the BF. Functionally, reovirus inoculation reduced both the response of PBLs to the phytohemagglutinin-P stimulation and monocyte uptake of latex beads. According to the protocols used here, no significant alteration in B-cell function could be detected in reovirus-infected chicks. With the exception of leukocyte hematology, IBDV-infected chicks had significantly altered responses in all tests used. By way of comparison, the effects of IBDV were more persistent and pronounced than were those seen with reovirus. The graft-versus-host reaction indicated an elevated and/or uninhibited response of T-cells in the blood of IBDV-infected chicks.

Animals↗

PubMedDate not supplied

Response of mibolerone-treated chickens to infectious bursal disease virus.

The response of mibolerone-treated chickens to infectious bursal disease virus (IBDV) was studied. Chickens fed a ration containing mibolerone at 1.5 parts per million (ppm) developed bursal atrophy by 4 weeks of age. No indication was found that mibolerone prevented IBDV infection even after 7 weeks of feeding. Furthermore, only chickens treated with mibolerone died when infected with IBDV at 2 or 3 weeks of age, and treated chickens had more severe clinical signs than did untreated controls when infected at 4-8 weeks of age. Chickens fed mibolerone had lower body weights than unmedicated controls, and apparently had a lower antibody response to IBDV and to bovine serum albumin.

Animals↗

PubMedDate not supplied

Infectious bursal disease virus: further characterization with evidence for a single-stranded RNA virus.

Infectious bursal disease virus (IBDV) that had been adapted to grow and was then cloned in chick embryo fibroblast (CEF) cell culture was examined for its physicochemical properties, the cellular site of virus replication, and the nature of its viral RNA. The IBDV was an RNA virus, acid-stable, absolutely resistant to chloroform, and moderately thermolabile. It appeared to replicate only in the cytoplasm, as shown by virus-specific antigens restricted to the cytoplasm of infected cells. The viral RNA was composed of single-stranded RNA, as evidenced by flame-red fluorescence on acridine-orange staining and an absence of specific fluorescence in infected cells on immunofluorescent staining with antiserum specific for double-stranded RNA. The IBDV virion had a hexagonal outline with an average diameter of 62 nm and possessed a single layer of capsid composed of hollow capsomeres without envelope. The buoyant density as determined in a continuous sucrose gradient was 1.178 g/cm3. The IBDV was found to possess morphologial and physicochemical properties different from those of any established RNA virus group.

Animals↗

PubMedDate not supplied

Responses of specific-pathogen-free chicks to concomitant infections of reovirus (WVU-2937) and infectious bursal disease virus.

Specific-pathogen-free white leghorn chicks concomitantly infected with both infectious bursal disease virus (IBDV) and reovirus (WVU-2937) on day 1 had significantly lower (P less than 0.05) virus-neutralizing- and precipitating-antibody geometric mean titers (GMT) to reovirus than chicks infected with only reovirus on day 1 but had a similar incidence of inflammation of the metatarsal digital flexor tendons. Chicks infected with IBDV on day 7 and reovirus on day 14 had a greater incidence of inflammation of the tarsometatarsal digital flexor tendons and lower neutralizing- and precipitating-antibody GMT to reovirus than chicks infected with only reovirus on day 14. Chicks infected with both viruses on day 1 had a significantly lower (P less than 0.05) neutralizing-antibody GMT to IBDV than chicks infected with only IBDV.

Animals↗

PubMedDate not supplied

Adaptation of the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay for the determination of virus-neutralizing antibodies using the virus-neutralization assay.

The tetrazolium salt MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide] has been widely used for bioassays. Herein is described the use of the MTT dye with a virus-neutralization (VN) assay to titer infectious bursal disease virus (IBDV)-neutralizing antibodies. A standard VN assay using chicken embryo fibroblasts (CEFs) and IBDV was used for the assessment of IBDV-neutralizing antibodies. The percent of CEF killing due to IBDV was quantitated using MTT, and the absorbance (A) data were used to calculate the VN antibody titer. This method of calculation offers the expression of VN titer in terms of units of activity per unit of volume.

Animals↗

PubMedDate not supplied

Infectious bursal disease viruses: molecular differentiation of antigenic subtypes among serotype 1 viruses.

Published nucleotide sequence data for IBDV variant viruses (A and 1048E) and classic viruses (STC, 52-70, PBG98, Cu-1, and 002-73) were used to identify restriction enzyme sites that could potentially be used to differentiate these strains of IBDV. To test this hypothesis, the genomes of IBDV strains STC, MD, NC, and OH were converted to cDNA using reverse transcriptase (RT) and then amplified using the polymerase chain reaction (PCR). The PCR primers were selected from relatively conserved sequence regions in the VP2 gene, and they were used to amplify a 394-base-pair fragment. The restriction enzymes (RE) DraI, EcoRII, SacI, Sau3AI, StyI, and TaqI were tested for their ability to digest the RT/PCR products. The STC classic virus was SacI-, StyI-, and EcoRII-positive and DraI-, Sau3AI-, and TaqI-negative. The MD, NC, and OH viruses were DraI-, Sau3AI-, and TaqI-positive and SacI-, StyI-, and EcoRII-negative. The classic STC strain could be differentiated from the variant MD strain using the RT/PCR-RE assay. Based on these results and the presence or absence of other restriction sites that were predicted by published nucleotide sequence data, the RT/PCR-RE assay has the potential to differentiate IBDV isolates MD, A, and 1048E. Published nucleotide sequence data and the RT/PCR-RE results obtained using STC and MD indicated that variant viruses MD, A, and 1048E could be differentiated from classic viruses STC, 52-70, PBG98, Cu-1, 002-73, and NC.

Animals↗

PubMedDate not supplied

Rapid and quantitative assay system for measuring anti-infectious bursal disease virus antibody using monoclonal antibody bound to polystyrene latex microspheres.

A monoclonal antibody (MAb) to infectious bursal disease virus (IBDV) that has virus-neutralizing activity was bound to polystyrene latex microspheres The microspheres agglutinated with extracts of bursae from chickens infected with IBDV. Agglutination was inhibited in a competitive manner by adding serum obtained from IBDV-infected chickens. The level of agglutination-inhibition depended on the serum antibody titer against IBDV. The reaction was visually accomplished within 5 minutes. The titer of this rapid assay showed a close relationship with that of the virus-neutralization test.

Animals↗

PubMedDate not supplied

Comparison of neutralizing epitopes among infectious bursal disease viruses using radioimmunoprecipitation.

Monoclonal antibodies (MAbs) were used to analyze the relatedness of neutralizing epitopes of infectious bursal disease virus (IBDV) strains. The MAb B69 neutralized the homologous D78 virus but not the MD and Del-A variant strains of IBDV. MAbs 33E8 and R63 neutralized D78 and variant strains MD and Del-A. A cDNA clone consisting of a 1000-base-pair fragment of the VP2 gene from the Del-A IBDV strain was translated using an in vitro system. Six peptides were observed following translation, which represented a full-length product (35.5 kilodaltons) and five truncated products. The translated peptides were radioimmunoprecipitated using MAbs B69, 33E8, and R63. Only MAb R63 immunoprecipitated the in vitro translation products from Del-A. MAbs B69 and 33E8 did not immunoprecipitate the in vitro-translated VP2 peptides. The D78 and Del-A viruses were radiolabeled in vivo using 35S-methionine. Proteins from these viruses were examined by radioimmuno-precipitation with MAbs B69, 33E8, and R63. Although the background made interpretation of the results difficult for MAb B69, this MAb clearly immunoprecipitated VP2 of D78. MAb 33E8 immunoprecipitated the D78 VP3 protein, and R63 immunoprecipitated the VP2 protein. MAb R63 also immunoprecipitated the 35S-methionine-labeled VP2 protein from Del-A. It was concluded that the neutralizing epitope represented by 33E8 was located on VP3 and that the epitope represented by R63 is located on both classic and variant viruses in the region of VP2 that is generally thought to contain sequence variability among IBDV strains.

Antigens, Viral↗

PubMedDate not supplied

Pathogenicity studies of an Arkansas variant infectious bursal disease virus.

A variant infectious bursal disease virus (IBDV), IBDV-s977, was blind passaged in cell culture, plaque purified, and attenuated by serial passage at a high multiplicity of infection (MOI) in chick embryo fibroblasts (CEF). Cell culture passages of virus caused less bursal atrophy and splenomegaly than did the original isolate and retained immunogenicity; however, virus tended to persist for a longer time in the bursa and spleen of birds infected with the highest CEF passages. Antibody to both low MOI and high MOI passages of IBDV-s977 poorly neutralized virus that was isolated from bursal tissue 28 days postinfection (PI). The spleens of chickens infected with the eighteenth CEF passage were negative for virus at 3 and 7 days PI but had high titers of virus at 14 and 28 days PI. There was also more virus in the bursa of birds infected with the fifteenth and eighteenth CEF passages at 28 days PI than at 7 or 14 days PI. Defective interference (DI) was demonstrated when cell cultures were coinfected with a constant amount of low MOI virus and serial dilutions of high MOI virus. There was an increase in interference score with increased passage number in CEF, and there was more interference in virus passaged at a high MOI. There was an inverse relationship between interference score and bursal lesion score and splenomegaly at 7 days PI, indicating that DI particles may be involved in virus attenuation. There was a positive relationship between interference and viral persistence in the bursa and spleen at 28 days PI. Antiserum to s977 was shown to enhance the nonlytic replication of s977 in CEF, presumably within macrophages, providing a possible mechanism for the pathotypic variation seen in emerging strains of IBDV.

Animals↗

PubMedDate not supplied

Restriction analysis of the MD infectious bursal disease virus strain.

The variant MD strain of infectious bursal disease virus (IBDV) was examined using restriction fragment length polymorphism (RFLP) and the molecular variation was compared with published sequences of both variant and classic IBDV strains. Viral RNA was transcribed into cDNA using reverse transcriptase and then amplified by the polymerase chain reaction (PCR). Three separate but overlapping fragments of 1603 bp, 1496 bp, and 1066 bp containing the entire coding region for VP2, VP4, and VP3, respectively, were amplified. These amplified products were initially cloned using the TA Cloning kit and further subcloned into the pGEM-3Zf and pUC19. Eight restriction enzymes, PstI, BamHI, AvaI, EcoRI, HindII, XmaI, SmaI, and XbaI, were tested for their ability to digest the MD PCR products. The resulting RFLP was analyzed and compared with the published genome segment A sequences of the classic IBDV strain STC and the variant IBDV strain GLS. Differences in restriction fragment profiles were observed after digestion with BamHI, EcoRI, XmaI, and SmaI, with the absence of the EcoRI site in both variant strains, GLS and MD. The MD PCR products lacked both XmaI and SmaI sites, which were present in both STC and GLS. The MD PCR products contained a BamHI site within the hypervariable region of VP2, which is present in STC but not in the variant GLS. An additional BamHI site was identified in the VP4 gene of MD and GLS but not in STC.

Animals↗

PubMedDate not supplied

Systemic and local antibody responses to infectious bronchitis virus in chickens inoculated with infectious bursal disease virus and control chickens.

Serum and local (respiratory) antibody responses to infectious bronchitis virus (IBV) were studied in 5-wk-old white leghorn-type control chickens and chickens inoculated with infectious bursal disease virus (IBDV) at 1 day of age. Of the chickens inoculated with IBV alone, 93% had detectable levels of IBV antibodies in the sera and 87% had detectable antibodies in the respiratory lavage fluids. Compared to this group, only 73% and 65% of IBDV-IBV inoculated chickens had serum and respiratory antibodies, respectively. In chickens inoculated with IBV alone, the IBV antibodies were evenly associated with immunoglobulin classes IgM, IgG, and IgA, whereas the IBDV-IBV inoculated chickens mainly produced IgM-associated antibodies with low to negligible levels of IgA- and IgG-associated antibodies. These results suggest that the lack of adequate IgA- and IgG-associated antibody production in IBDV-infected chickens may account for their increased susceptibility to IBV infection.

Animals↗

PubMed1999

Chimeric infectious bursal disease virus-like particles expressed in insect cells and purified by immobilized metal affinity chromatography.

Chimeric virus-like particles (VLPs) of infectious bursal disease virus (IBDV) were produced by coinfecting Spodoptera frugiperda (Sf-9) insect cells with two recombinant baculoviruses, vIBD-7 and vEDLH-22. vIBD-7 encodes VP2, VP3, and VP4 of the IBDV structural proteins. vEDLH-22 encodes VP2 with five histidine residues at the carboxy-terminus (VP2H). Coinfection produced hybrid VLPs composed of VP2, VP2H, and VP3. The additional histidine residues on VP2H enabled the efficient purification of VLPs based on immobilized metal affinity chromatography (IMAC). These results demonstrated that the VLPs formed are comprised of chimeric subunits with attached affinity ligands, and further, that sufficient His5 ligand was available for binding to the IMAC metal-chelating resin. Additionally, these novel particles were fully characterized for antigenicity by a series of monoclonal antibodies, and appeared identical to the two wild-type IBDV strains contributing subunits to the chimeric VLP. IMAC purification provides a promising low-cost and simple scheme to purify VLPs as vaccines.

Animals↗

PubMed1999

Proteolytic processing in infectious bursal disease virus: identification of the polyprotein cleavage sites by site-directed mutagenesis.

The infectious bursal disease virus (IBDV), a member of the Birnaviridae family, is the causative agent of an immune depressive disease that affects domesticated and wild avian species. The expression strategy of IBDV includes the synthesis of a 110-kDa polyprotein containing the capsid precursor polypeptides. The polyprotein is autocatalitically processed rendering three polypeptides: NH2-VPX-VP4-VP3-COOH. We have carried out a systematic analysis, using a series of plasmids encoding polyproteins containing either deletions or single amino acid substitutions, to identify the processing sites. The results obtained showed the existence of two sites, 511LAA513 and 754MAA756, that are essential for the processing of the VPX-VP4 and VP4-VP3 precursors, respectively. These sequences are highly conserved among IBDV strains form serotypes 1 and 2. A secondary VPX-VP4 processing site was detected in a 19-amino acid stretch located upstream of the 511LAA513 site. Analyses using versions of the 754MAA756 VP4-VP3 processing site containing conservative and nonconservative amino acid substitutions demonstrated that the specificity of the cleavage is dictated by the conserved AA dipeptide.

Amino Acid Sequence↗