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PubMed1995

Identification of a novel viral protein in infectious bursal disease virus-infected cells.

Infectious bursal disease virus (IBDV), a member of the Birnaviridae, specifies two genomic double-stranded RNAs, segment A and segment B. Segment A encodes a 110 kDa polyprotein which is processed into virus proteins VP2, VP3 and VP4. A second open reading frame (ORF), designated ORF A-2, immediately preceding and partially overlapping the 110 kDa protein gene has also been described. After prokaryotic expression of this ORF and immunization of rabbits with the expressed protein we obtained reagents that allowed the identification of the ORF A-2 gene product in IBDV-infected cells. The ORF A-2 protein exhibits an apparent molecular mass of 21 kDa which is larger than the size of 16.5 kDa calculated from the deduced amino acid sequence. Immunofluorescence studies demonstrated the presence of the ORF A-2 protein in bursa samples from IBDV-infected chicken. In summary, the IBDV ORF A-2 product represents the fifth IBDV protein described. Therefore, we propose to designate it as IBDV VP5.

Animals↗

PubMed2000

Role of Ser-652 and Lys-692 in the protease activity of infectious bursal disease virus VP4 and identification of its substrate cleavage sites.

The polyprotein of infectious bursal disease virus (IBDV), an avian birnavirus, is processed by the viral protease, VP4. Previous data obtained on the VP4 of infectious pancreatic necrosis virus (IPNV), a fish birnavirus, and comparative sequence analysis between IBDV and IPNV suggest that VP4 is an unusual eukaryotic serine protease that shares properties with prokaryotic leader peptidases and other bacterial peptidases. IBDV VP4 is predicted to utilize a serine-lysine catalytic dyad. Replacement of the members of the predicted catalytic dyad (Ser-652 and Lys-692) confirmed their indispensability. The two cleavage sites at the pVP2-VP4 and VP4-VP3 junctions were identified by N-terminal sequencing and probed by site-directed mutagenesis. Several additional candidate cleavage sites were identified in the C-terminal domain of pVP2 and tested by cumulative site-directed mutagenesis and expression of the mutant polyproteins. The results suggest that VP4 cleaves multiple (Thr/Ala)-X-Ala downward arrowAla motifs. A trans activity of the VP4 protease of IBDV, and also IPNV VP4 protease, was demonstrated by co-expression of VP4 and a polypeptide substrate in Escherichia coli. For both proteases, cleavage specificity was identical in the cis- and trans-activity assays. An attempt was made to determine whether VP4 proteases of IBDV and IPNV were able to cleave heterologous substrates. In each case, no cleavage was observed with heterologous combinations. These results on the IBDV VP4 confirm and extend our previous characterization of the IPNV VP4, delineating the birnavirus protease as a new type of viral serine protease.

Amino Acid Sequence↗

PubMed2001

VP5 and the N terminus of VP2 are not responsible for the different pathotype of serotype I and II infectious bursal disease virus.

Two serotypes have been identified in infectious bursal disease virus (IBDV), a member of the family BIRNAVIRIDAE: A reverse genetics system was used for generation of chimeras in genome segment A of the two serotypes, in which the complete viral VP5 gene and 3' noncoding region (NCR), or parts thereof, were exchanged. The engineered viruses were characterized in vitro and in vivo in comparison to serotype I and II IBDV. Our results show that IBDV chimeras exhibit a different phenotype in cell culture compared to the wild-type viruses. In in vitro-cultivated bursal-derived cells, chimeric viruses infected B lymphocytes, as does serotype I IBDV. Surprisingly, serotype II virus was also able to infect in vitro-cultivated bursal cells, but these were neither B lymphocytes nor macrophages. After infection of susceptible chickens all chimeras replicated in the bursa of Fabricius (BF), and three chimeric viruses caused mild depletion of bursal cells. In contrast, after infection of chickens with a chimeric IBDV containing exchanged VP5 as well as 3'-NCR, no depletion was detectable. The serotype II strain did not replicate in the BF nor did it cause depletion of bursal cells. Thus, the origin of VP5 does not explain the different pathotype of IBDV serotype I and II.

3' Untranslated Regions↗

PubMed1997

Passive protection of specific pathogen free chicks against infectious bursal disease by in-ovo injection of semi-purified egg-yolk antiviral immunoglobulins.

In order to develop an experimental model for passive immunity in SPF chickens, active neutralizing immunoglobulins (Ig) directed against infectious bursal disease virus (IBDV) were extracted from the yolk of eggs laid by conventional layers immunized against IBDV. Concentrated Ig extracts were inoculated via the intra-vitellin route into 7-day-old embryonated SPF hen eggs. Although detrimental to hatchability, Ig inoculation resulted in hatching two series of SPF chicks with passive immunity against IBDV. The neutralizing and ELISA antibody titres at 1 day-old (respectively 12.64 and 13.15 log2; and 4915 and 4277), the kinetics of decay of the anti-IBDV antibodies and the protection afforded by passive antibodies against highly virulent IBDV challenge proved highly consistent with data previously reported on conventional chicks. In-ovo inoculation of purified egg-yolk immunoglobulins may hence be a good experimental model for anti-IBDV maternally-transmitted immunity. This experimental model might possibly be adapted to other pathogens or vaccines for which interference with maternally derived antibodies is a matter of concern at 1 day-old.

Animals↗

PubMed1978

Interaction between infectious bursal disease virus and Newcastle disease virus in chickens.

The Australian strain of infectious bursal disease virus (IBDV), 002/73, affected the response of chickens to Newcastle disease virus (NDV). The titre of serum antibodies to NDV in chickens infected with IBDV was significantly lower than that of birds infected with NDV alone. It also appeared that IBDV affected NDV excretion from chickens as NDV was more frequently isolated from chickens infected with IBDV, IBDV infection did not alter the pathogenicity of NDV in chickens. This Australian strain of IBDV therefore appeared to be immunodepressive in one-day-old chickens.

Animals↗

PubMed1989

Detection of infectious bursal disease viruses by using cloned cDNA probes.

A molecular clone representing 445 base pairs at the 3' end of infectious bursal disease virus (IBDV) genome segment B was used in a dot blot hybridization assay to detect viral RNA from cell culture and from chicken bursa and spleen tissue specimens. The cloned nucleotide sequence represents approximately 14% of the virus-encoded polymerase (VP-1) gene. The lower detection limit of radiolabeled probes prepared from this clone was 0.1 ng of IBDV double-stranded RNA. The probe had broad specificity and was used to detect four serotype 1 IBDV strains and one serotype 2 IBDV strain. This probe, however, did not cross-react with nucleic acid extracted from nine unrelated poultry viruses. A rapid procedure for isolation of IBDV genomic RNA from bursa and spleen tissue specimens was developed and used with the dot blot hybridization assay to detect IBDV strains in tissue samples from experimentally infected and commercially reared chickens.

Animals↗

PubMed1994

Single-tube, noninterrupted reverse transcription-PCR for detection of infectious bursal disease virus.

An assay protocol based on single-tube, noninterrupted reverse transcription-PCR (RT-PCR) for the detection of infectious bursal disease virus (IBDV) is described. After the conditions for RT-PCR had been optimized, a primer set framing a region within the gene coding for IBDV VP2 protein was used to amplify a 318-bp fragment of the IBDV genome. Amplified product was detected with three strains of IBDV, whereas none was obtained from uninfected bursal tissue or seven unrelated avian viruses. The sensitivity of this RT-PCR was tested with purified viral RNA from three strains of IBDV. The detection limit was 10 fg in an ethidium bromide-stained gel. In addition, this assay system was used to detect IBDV in bursal-tissue specimens from commercially reared chickens. The identity of the amplified products from the tissue specimen preparation was determined by using a rapid, simple procedure in which internally nested, end-labeled probes were used.

Animals↗

PubMed1997

VP5 of infectious bursal disease virus is not essential for viral replication in cell culture.

Infectious bursal disease virus (IBDV), a member of the Birnaviridae family, encodes in its bisegmented double-stranded RNA genome four structural virion proteins, VP1, VP2, VP3, and VP4, as well as a nonstructural protein, VP5. Recently, the establishment of an infectious cRNA system for IBDV has been described (E. Mundt and V. N. Vakharia, Proc. Natl. Acad. Sci. USA 93:11131-11136, 1996). Here, we report the isolation of a VP5- IBDV mutant constructed by site-directed mutagenesis of the methionine start codon of VP5, followed by cRNA transfection. The resulting virus mutant was replication competent in cell culture, which indicates that VP5 is not required for productive replication of IBDV. Absence of VP5 expression was verified by lack of reactivity with newly established anti-VP5 monoclonal antibodies and polyclonal sera. VP5- IBDV exhibited a delay in replication in chicken embryo cells compared to the VP5+ parental virus. However, final yields were similar. Our results thus show that VP5 is nonessential for IBDV replication, which makes it a prime candidate for the construction of deleted, marked vaccines.

Amino Acid Sequence↗

PubMed1998

Generation of a mutant infectious bursal disease virus that does not cause bursal lesions.

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.

Animals↗

PubMed1999

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.

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.

Animals↗

PubMed2001

Molecular determinants of virulence, cell tropism, and pathogenic phenotype of infectious bursal disease virus.

Infectious bursal disease viruses (IBDVs), belonging to the family Birnaviridae, exhibit a wide range of immunosuppressive potential, pathogenicity, and virulence for chickens. The genomic segment A encodes all the structural (VP2, VP4, and VP3) and nonstructural proteins, whereas segment B encodes the viral RNA-dependent RNA polymerase (VP1). To identify the molecular determinants for the virulence, pathogenic phenotype, and cell tropism of IBDV, we prepared full-length cDNA clones of a virulent strain, Irwin Moulthrop (IM), and constructed several chimeric cDNA clones of segments A and B between the attenuated vaccine strain (D78) and the virulent IM or GLS variant strain. Using the cRNA-based reverse-genetics system developed for IBDV, we generated five chimeric viruses after transfection by electroporation procedures in Vero or chicken embryo fibroblast (CEF) cells, one of which was recovered after propagation in embryonated eggs. To evaluate the characteristics of the recovered viruses in vivo, we inoculated 3-week-old chickens with D78, IM, GLS, or chimeric viruses and analyzed their bursae for pathological lesions 3 days postinfection. Viruses in which VP4, VP4-VP3, and VP1 coding sequences of the virulent strain IM were substituted for the corresponding region in the vaccine strain failed to induce hemorrhagic lesions in the bursa. In contrast, viruses in which the VP2 coding region of the vaccine strain was replaced with the variant GLS or virulent IM strain caused rapid bursal atrophy or hemorrhagic lesions in the bursa, as seen with the variant or classical virulent strain, respectively. These results show that the virulence and pathogenic-phenotype markers of IBDV reside in VP2. Moreover, one of the chimeric viruses containing VP2 sequences of the virulent strain could not be recovered in Vero or CEF cells but was recovered in embryonated eggs, suggesting that VP2 contains the determinants for cell tropism. Similarly, one of the chimeric viruses containing the VP1 segment of the virulent strain could not be recovered in Vero cells but was recovered in CEF cells, suggesting that VP1 contains the determinants for cell-specific replication in Vero cells. By comparing the deduced amino acid sequences of the D78 and IM strains and their reactivities with monoclonal antibody 21, which binds specifically to virulent IBDV, the putative amino acids involved in virulence and cell tropism were identified. Our results indicate that residues Gln at position 253 (Gln253), Asp279, and Ala284 of VP2 are involved in the virulence, cell tropism, and pathogenic phenotype of virulent IBDV.

Amino Acid Sequence↗

PubMed1993

Chemiluminescent detection of infectious bursal disease virus with a PCR-generated nonradiolabeled probe.

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 10-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.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Proventriculitis in broiler chickens: effects of immunosuppression.

Proventriculitis in broilers causes carcass condemnation when swollen proventriculi tear during evisceration. The cause of this proventriculitis is unknown, but several infectious agents have been associated with it. One such agent, infectious bursal disease virus (IBDV), has been implicated as a cause of proventriculitis, but a direct effect of this virus on the proventriculus has not been proven. The role of IBDV in proventriculitis may be indirect as a result of its ability to cause immunosuppression. The objective of this study was to understand how immunosuppression affects the incidence of proventriculitis in broiler chickens. Immunosuppression was induced in commercial and specific-pathogen-free broiler chickens using chemicals (cyclophosphamide and cyclosporin) or virus (IBDV). All groups were then exposed to a proventricular homogenate produced from diseased birds. At 7 and 14 days postinoculation, the incidence of proventriculitis in these groups was compared to that produced by homogenate exposure in immunocompetent broilers. All birds exposed to the proventricular homogenate from diseased birds developed proventriculitis. Cyclophosphamide and IBDV, both B cell suppressors, did not significantly affect the incidence or characteristics of the proventriculitis observed, although they did have an effect on the size of the proventriculus at 7 days postinoculation. Chickens immunosuppressed with cyclosporin, a T cell suppressor, developed more severe lesions and had a higher incidence of proventriculitis. These findings indicate that both B and T cells are involved in the immune response against proventriculitis, but cell-mediated immunity appears to have a more important role in controlling the disease. IBDV affects both humoral and cellular immunity in the chicken, so although under experimental conditions it didn't have a major effect on proventriculitis, it may explain why control of IBDV in the field seems to reduce the incidence of proventriculitis.

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PubMed2004

A very virulent genotype of infectious bursal disease virus predominantly associated with recurrent infectious bursal disease outbreaks in Tunisian vaccinated flocks.

Outbreaks of infectious bursal disease (IBD) still continue to afflict the Tunisian poultry industry even in those flocks where the vaccination program is strictly applied. To characterize the viruses that circumvent protection provided by vaccination, field isolates of infectious bursal disease virus (IBDV) obtained from vaccinated flocks that have repeatedly experienced IBDV outbreak episodes were analyzed from bursal samples by reverse transcription coupled with polymerase chain reaction and dideoxynucleotide sequencing of the VP2 hypervariable region. Although sequence data were obtained from samples collected from three distinct flocks over a period of 3 years, only limited sequence variation has been observed. The few nucleotide changes were silent and the deduced amino acid sequences were identical. Thus, the virus population that predominates in the field seems to represent a homogeneous antigenic pool. Compared with the VP2 sequences of several IBDV strains, this predominant pool was found to be closely related to the very virulent (vv) IBDV viruses described in Europe and Asia. Sequence and phylogenetic analysis of the precursor polyprotein coding sequence of a representative Tunisian isolate further confirmed its assignment to the vv genotype. The deduced amino acid sequence of the whole polyprotein of the Tunisian isolate was found to be identical to a South Korean IBDV strain. Alignment of the polyprotein amino acid sequence of 35 IBDV strains identified additional mutations outside the VP2 variable domain and which occur frequently in vv strains. Based on this comparative analysis, the set of amino acid residues that should represent a typical vv profile involves Ala222, Ile242, Ile256, Ile294, Leu451, Tyr680, N685, Ser715, Asp751, Val990, and Ala1005. Such a combination of amino acid changes was observed for the majority of vvIBDV strains that define a distinct phylogroup.

Amino Acid Sequence↗

PubMed2005

Molecular epidemiology of infectious bursal disease viruses: distribution and genetic analysis of newly emerging viruses in the United States.

Genetic mutations in the genome of infectious bursal disease virus (IBDV) have resulted in antigenic and pathogenic variants that continue to cause disease in commercially reared chickens. The extent of the genetic diversity among IBDV strains circulating in the United States is unknown. This study was designed to identify newly emerging viruses infecting chickens on poultry farms experiencing immune suppression-related problems. Fifty IBDV-positive samples were identified from 273 bursa samples using a real-time reverse transcription-polymerase chain reaction (RT-PCR) assay. Mutation probes were designed to the hydrophilic B coding region of the VP2 gene. Six mutation probes used in this study were based on the nucleotide sequences of the Del-E, Bursine 2, D-78, STC, G6, and T1 IBDV strains. Following real-time RT-PCR, these mutation probes identified 11 of the 50 viruses in the melting temperature (Tm) analysis. The results indicated that the remaining 39 viruses had one or more nucleotide mutations compared with the six mutation probes in this region of the VP2 gene. Thirty-eight viruses were chosen for nucleotide sequence analysis across the hypervariable region of the VP2 gene. Within this group of 38 viruses, four were identified by the mutation probes and their nucleotide sequences confirmed that real-time RT-PCR data. In the remaining 34 viruses, nucleotide mutations were observed in as many as 8 of 23 nucleotides across the hydrophilic B epitope coding region. Furthermore, every amino acid position except one between 316 and 324 had at least one substitution mutation. Phylogenic analysis placed two of the 38 viruses sequenced on branches with classic viruses and the remaining 36 viruses were placed on four distinct branches. Branches 1 and 2 contained a majority of the viruses, which were distributed across most of the major poultry-producing states in the United States. These branches contained previously characterized variant IBDV strains. Viruses in branches 3 and 4 were confined to three states and did not contain any previously characterized IBDV strains.

Animals↗

PubMed2005

Viral genotyping of infectious bursal disease viruses isolated from the 2002 acute outbreak in Spain and comparison with previous isolates.

An infectious bursal disease (IBD) outbreak occurred in the east region of Spain in the spring of 2002 and rapidly spread thorough the whole country, although proper vaccination programs were applied. In this report, 33 infectious bursal disease viruses (IBDVs) isolated from this outbreak were characterized by nucleotide sequencing of the VP2 gene hypervariable region and were compared with reference IBD strains and the 1990s Spanish IBDVs in order to determine possible emergence of IBDV isolates with modified antigenic or virulent properties. Moreover, histopathologic and immunohistochemical studies of those cases where bursal tissues were available were carried out. Of the 33 isolates, 23 were identified as very virulent IBDVs (vvIBDVs), whereas the other 10 isolates were classified as attenuated or intermediate virulence classical strains and could possibly be IBDV live vaccine strains used in the immunization of these chickens. Results of this study indicate that wIBDV isolates from the 2002 Spanish outbreak are closely related with those from the 1990s outbreak. However, acute IBD cases have not been reported in Spain during these 10 yr. Genetic, management, and environmental factors likely related with IBD reemergence in Spain are discussed. Moreover, our results indicate that good correlation exists between the IBDV subtype present in the field and the degree of lesions in bursa tissue, as well as the immunohistochemistry staining.

Amino Acid Sequence↗

PubMedDate not supplied

Failure of viral protein 3 of infectious bursal disease virus produced in prokaryotic and eukaryotic expression systems to protect chickens against the disease.

In recent years, infectious bursal disease virus (IBDV) has become a serious economic problem as a result of the emergence of new and very virulent strains. Most of the antibodies produced against IBDV are for the structural proteins viral protein (VP) 2 (VP2) and VP3. The purpose of this study was to test the potential of recombinant VP3 to induce protective antibodies. The gene for VP3 was isolated from a virulent strain of the virus and cloned into prokaryotic (Escherichia coli) and eukaryotic (baculovirus) expression systems. The protein expressed by both systems was of the expected size (32 kD) and was detected by anti-IBDV antibodies. Following partial purification, the polypeptides were injected into intact birds and induced the production of high levels of anti-IBDV antibodies, as detected by immunoblot and enzyme-linked immunosorbent assay tests. These antibodies did not prevent changes in the bursa and mortality when birds were challenged with a virulent IBDV strain after vaccination with the recombinant VP3. The results show that VP3 polypeptide cannot be used as a subunit vaccine against IBDV and raise questions concerning the nature of the neutralizing epitope on this structural protein.

Animals↗

PubMed1999

Response of embryonic chicken lymphocytes to in ovo exposure to lymphotropic viruses.

OBJECTIVE: To examine effects of virus exposure on embryonic lymphoid organ structure, apoptosis, and lymphoid cell subpopulations. ANIMALS: Eggs of specific pathogen free (SPF) White Leghorn chickens at embryonation day (ED) 17. PROCEDURES: Eggs were inoculated with 2,000 plaque-forming units (PFU) of serotype 1 herpesvirus (Marek's disease virus [MDV 1]), 2,000 PFU of herpesvirus of turkeys (MDV 3), or 1,000 embryo infectious doses (EID50) of infectious bursal disease virus (IBDV). On post-inoculation days (PID) 3 and 5, lymphoid organ to body weight ratios were determined, and bursa of Fabricius, thymus, and spleen were evaluated for lesions and apoptosis. Proportions of lymphoid cell subpopulations of PID-3 chicken embryos and 7- to 10-day-old chicks were quantitated by flow cytometry. RESULTS: Lymphoid organ weights were similar in virus-free, MDV1, and IBDV groups. Embryos inoculated with 2,000 PFU MDV 3/egg had lower bursal weights than virus-free controls. In a repeated trial, MDV 3 (1,000 PFU to 4,000 PFU) did not reduce bursal weights among groups. Histologic changes were seen in bursae after MDV 1 and IBDV inoculation. Apoptosis was greater in bursae of MDV 1-infected embryos than controls. Lymphoid cell subpopulations were similar among all groups with the exception of CD8+ and IgM+ cells in spleens of IBDV-infected 10-day-old chicks. CONCLUSIONS AND CLINICAL RELEVANCE: Infection with pathogenic strains of MDV 1 and IBDV did not alter lymphocyte subpopulations in embryos or cause complete destruction of lymphoid organs. Changes in lymphoid cell subpopulations exposed as embryos to IBDV were seen only after hatching.

Animals↗