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PubMed2004

Sequence analysis of the variable VP2 gene of infectious bursal disease viruses passaged in Vero cells.

Korean field infectious bursal disease viruses (IBDVs) were isolated from IBDV suspected commercial chickens. A previous study revealed that these IBDV field isolates were virulent or very virulent IBDVs. The isolates were passaged three times in the chorioallantoic membrane of specific-pathogen-free embryonated chicken eggs and four times in Vero cells. After passage, viral RNAs were isolated and purified to determine the genetic changes. The hypervariable regions of the VP2 gene were amplified by reverse transcriptase-polymerase chain reaction (RT-PCR). To confirm the genetic changes, PCR products were cloned, sequenced and compared to the sequences of the parental IBDVs and published IBDV strains. By sequencing analysis, the passaged IBDVs had amino acid changes at positions 253 (Q --> H), 279 (D or N --> N) and 284 (A --> T) which were commonly found in the attenuated IBDV strains. Two serines in the serine-rich heptapeptide (residue 326-332) were substituted into other amino acids which were similar to the IBDV vaccine strains.

Amino Acid Sequence↗

PubMed2006

Chicken recombinant antibodies against infectious bursal disease virus are able to form antibody-virus immune complex.

Virus particles exposed to specific anti-virus antibodies result in the formation of immune complexes (Icx). Recent vaccination strategies have employed this feature, and an infectious bursal disease virus (IBDV) vaccine based on Icx has been released and is expected to replace conventional IBDV vaccines. We evaluated whether chicken recombinant antibodies (rAb) specific for IBDV, rather than conventional chicken anti-IBDV sera, could be used to generate Icx. Out of 14 rAb expressed as soluble single-chain variable fragments (scFv), nine were able to completely neutralize Bursavac, a live IBDV vaccine, when tested in ovo. When these rAb were mixed with IBDV and inoculated into either 18-day-old embryos, or 1-day-old or 2-week-old specific pathogen free chicks, a rAb.IBDV complex was formed. These Icx were similar to those produced by polyclonal chick anti-IBDV sera and IBDV. Following inoculation of the rAb.IBDV complex, the virus was rendered non-infectious for 5 to 7 days. After this time virus was released from the Icx, resulting in infection of the inoculated chicks and subsequent induction of an immune response and protection against virulent IBDV challenge. The results indicated that genetically derived antibodies can replace polyclonal sera in the formulation of Icx vaccines.

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PubMed1996

Enzyme-linked immunosorbent assay-based detection of antibodies to antigenic subtypes of infectious bursal disease viruses of chickens.

An enzyme-linked immunosorbent assay (ELISA) using a fragment of the infectious bursal disease virus (IBDV) VP2 gene expressed in baculovirus was developed. A 944-bp portion of the VP2 gene from the Del-A strain of IBDV was ligated into the pAc360 transfer vector and transfected into baculovirus, Recombinant baculoviruses were identified by dot blot hybridization. The recombinant baculovirus 9A5 expressed a 57-kDa VP2 fusion protein, which was immunoprecipitated. This baculovirus-expressed VP2 was used as an antigen in an ELISA (Ohio State University [OSU]-ELISA). Titers of sera from specific-pathogen-free chickens infected with different strains of IBDV in our laboratory were determined by the OSU-ELISA, commercial ELISAs, and a virus neutralization assay. The results indicate that all sera from the specific-pathogen-free chickens infected with IBDV strains contained high titers of neutralizing antibodies. Each of these antisera also tested positive with the commercial ELISA kits. The OSU-ELISA did not detect antibodies to all strains of IBDV tested. This ELISA detected antibodies to the antigenically similar Delaware variant strains Del-A, Del-E, and GLS but did not detect or detected very poorly antibodies to antigenically heterologous classic IBDV strains STC, D78, and BVM. Although the antiserum to the IN strain of IBDV contained a virus-neutralizing antibody titer, the OSU-ELISA did not detect antibodies in this serum, suggesting IN is antigenically heterologous to Del-A. Titers to the IN strain were detected with the commercial ELISA kits. The OSU-ELISA detected antibodies to the SAL strain, suggesting this virus is antigenically similar to Del-A, which is supported by previously reported vaccination and challenge studies. In conclusion, the OSU-ELISA could be used to detect antibodies to a subgroup of IBDV strains, while commercially available ELISA kits detected antibodies to all the antigenic subtypes of IBDV tested.

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PubMed1980

Comparison of inactivated and live infectious bursal disease virus vaccines in White Leghorn breeder flock.

Leghorn breeder chickens, which had received live infectious bursal disease (IBDV) virus vaccine at 12 weeks of age and had been injected subcutaneously at 20 weeks of age with an inactivated IBDV oil emulsion vaccine, produced very high antibody titers which persisted for at least 9 months and were more uniform than those obtained from breeders receiving only the live IBDV vaccine. Breeders vaccinated with the inactivated IBDV oil emulsion vaccine at 12 and 20 weeks of age had antibody titers higher than breeders which received only the live IBDV vaccine at 12 weeks of age; titers were lower than in the group which received both the live and inactivated oil emulsion IBDV vaccines. Maternal antibody levels in chickens derived from parent flocks vaccinated with the inactivated oil emulsion IBDV vaccine were higher and more uniform than in chickens derived from parent flocks vaccinated with the live IBDV vaccine. Maternal antibody persisted longer in chickens derived from parent flocks vaccinated at 20 weeks of age with the inactivated oil emulsion IBDV vaccine than in chickens vaccinated by the other procedures. The titers remained quite high up to 16 days of age.

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PubMedDate not supplied

Recovery of antibody-producing ability and lymphocyte repopulation of bursal follicles in chickens exposed to infectious bursal disease virus.

We studied the long-term effect of infectious bursal disease virus (IBDV) in chickens. Specifically, the restoration of virus-induced bursal lesions and the duration of humoral immunodeficiency were examined. One-week-old specific-pathogen-free chickens were intraocularly inoculated with an intermediate vaccine strain (IBDV-Vac) or a virulent strain (IM-IBDV). At intervals postinoculation (PI), chickens were examined for histopathologic lesions. At 1, 3, 5, 10, or 15 wk PI, the chickens were injected with a mixture of antigens, and primary antibody responses were examined at 10 days postimmunization. Initially, the virus caused extensive necrosis of bursal B lymphocytes. This lesion was accompanied by an infiltration of T lymphocytes. With time, the necrotic lesion in the bursa was resolved. The follicles became partly repopulated with B lymphocytes. The repopulation occurred faster in the chickens exposed to IBDV-Vac than in the chickens exposed to IM-IBDV. By 7 wk PI, 40% and 80% of bursal follicles in IM-IBDV- and IBDV-Vac-inoculated chickens, respectively, were repopulated with immunoglobulin M+ B lymphocytes. Both IBDV-Vac and IM-caused suppression of the primary antibody response to antigens. However, the antibody responses of the chickens exposed to either of the two IBDV strains used were compromised only during the first 6 wk of virus exposure. Subsequently, the antibody response returned to near normal levels.

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PubMedDate not supplied

Molecular detection of infectious bursal disease virus by polymerase chain reaction.

The polymerase chain reaction (PCR) technique was applied to the detection of infectious bursal disease virus (IBDV). Reverse transcription followed by the PCR was used to amplify a portion of IBDV genome. A set of primers that specify a 150-base-pair segment of IBDV genome was chosen from an Australian strain of IBDV. Standard challenge strain and variant strains A, D, E, G, and GLS-5 of IBDV serotype 1 and OH strain of serotype 2 from infected bursae were subjected to reverse transcription, followed by 30 cycles of PCR. A single band of the PCR product (DNA) of the expected size from each strain of IBDV was visible on polyacrylamide gels stained with ethidium bromide. Using the same primers, no PCR product was detected from genomic nucleic acids of turkey hemorrhagic enteritis virus, infectious bronchitis virus, reovirus, Salmonella enteritidis, Escherichia coli, and uninfected bursae. The PCR could be efficiently performed on serially diluted IBDV RNA and could detect 2 femtograms of IBDV RNA. The identity of the PCR products was confirmed by direct sequencing. The PCR is a specific and sensitive method for the detection of IBDV.

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PubMedDate not supplied

Response to several avian respiratory viruses as affected by infectious bursal disease virus.

After being inoculated with the infectious bursal disease virus (IBDV) at one day of age, specific-pathogen-free chickens were inoculated with either Newcastle disease virus (NDV), infectious bronchitis virus (IBV), or infectious laryngotracheitis virus (ILTV). Their immunity was challenged 2-3 weeks later with homologous virus, and antibody titers were determined for ILTV and IBV. Several studies were made to determine the effects of IBDV on the development of persistent or chronic virus infections. Chickens susceptible to IBDV were exposed to IBDV at one day and inoculated at two weeks of age with either NDV, IBV, or ILTV. Two, three, four, and five weeks postinoculation with the respiratory viruses, tracheal swabbings were collected for virus isolations. The birds were challenged with homologous virus at five weeks postinoculation. The results show that early (1-day) infections with IBDV affect the response of young birds to several avian respiratory viruses, as indicated by lowered resistance to challenge and humoral antibody levels for birds inoculated with ILTV and NDV. Birds infected with IBV and IBDV withstood IBV challenge but were much more prone to persistent infections than were birds not exposed to IBDV. High death rates and decreased weights in all IBDV-inoculated groups demonstrated the damaging effects of early IBDV infection.

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PubMedDate not supplied

Experimental infection of turkeys with infectious bursal disease virus.

Commercial turkey poults 3 to 6 weeks old were infected experimentally by eyedrop with an infectious bursal disease virus (IBDV) inoculum obtained from chickens experiencing clinical IBD. The IBDV was passed 6 successive times in poults in an attempt to increase its pathogenicity for turkeys. Regardless of passage level, the IBDV infection in poults was subclinical, with no morbidity, mortality, or gross lesions observed. The bursae of Fabricius from infected poults, however, displayed various degrees of microscopic degeneration and IBDV specific fluorescence at 3, 4, and 5 days postinfection (PI). Infected turkeys also developed low levels of virus-neutralizing antibodies against IBDV at 12 days PI. Uninoculated poults kept in the same unit with infected poults also displayed microscopic changes and IBDV specific fluorescence 7 days after their appearance in inoculated poults. The IBDV was isolated from infected poults only after 5 successive passages of bursal material from infected poults in 9-day-old chick embryos. The IBDV from infected embryos was inoculated into susceptible 3-week-old chickens and 5-week-old poults and produced IBDV fluorescence and microscopic pathology in the bursae of infected poults and clinical IBD in infected chickens.

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PubMedDate not supplied

Serologic evidence of infectious bursal disease virus infection in Iowa turkeys.

Two infectious bursal disease viruses (IBDVs)--a cell-culture-adapted chicken strain designated Edgar strain and a recent isolate from turkeys in Missouri--were used to assay sera from 10 Iowa turkey flocks collected between 1 and 16 weeks of age. The two viruses were serologically distinct in cross-neutralization tests. For all flocks, a similar serologic pattern was found consisting of (1) low maternal antibody titers to turkey IBDV and occasionally to Edgar strain IBDV between 1 and 3 weeks of age, (2) a period of very low or no detectable titers between 3 and 7 weeks of age, and (3) sharply rising high titers to turkey IBDV with low titers to Edgar IBDV beginning at 5 to 8 weeks of age. These findings indicate that infection with IBDV of the serotype represented in this study by the turkey isolate is common in Iowa turkey flocks, whereas infection with IBDV represented by Edgar strain is uncommon. Infection occurred between 3 and 7 weeks of age during the late brooding period or after birds had been moved to an intermediate growing facility. All flocks developed complicated respiratory disease with excessive mortality caused by Escherichia coli septicemia, typically between 3 and 6 weeks of age. Although there was a temporal relationship between IBDV infection and respiratory disease, the possible role of IBDV in the process is unknown.

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PubMedDate not supplied

Pathogenicity and persistence of Salmonella enteritidis and egg contamination in normal and infectious bursal disease virus-infected leghorn chicks.

The pathogenicity and persistence of Salmonella enteritidis (SE) phage type 8 and resulting egg contamination in normal and infectious bursal disease virus (IBDV)-infected white leghorn chicks were evaluated over 34 weeks and in some birds over a 64-week period. Four hundred 1-day-old specific-pathogen-free (SPF) straight-run white-leghorn chickens were allotted into four treatment groups: negative control, IBDV-infected, IBDV+SE-infected, and SE-infected. Chicks were infected with IBDV at 1 day of age and with SE phage type 8 at 2 days of age. SE persisted in the gut of more than 50% of the chicks of both SE-infected groups through 34 weeks postinoculation (PI), and SE could still be isolated from cloacal/rectal swabs taken at 64 weeks. IBDV+ SE-infected chicks had severe gross lesions and significantly (P < 0.001) higher mortality (32%) than the negative control (1%), IBDV-infected (10%), and SE-infected (1%) groups. Gross lesions consisting of fibrinous pericarditis, perihepatitis, peritonitis, airsacculitis, and inspissated yolk were observed only in the IBDV+SE-infected group. SE isolations from internal organs of chickens in the IBDV+SE-infected group decreased from 83% at 8 weeks to 0% at 14 weeks PI; isolations from the SE-infected group decreased from 50% at 8 weeks to 0% at 10 weeks PI. Salmonella isolations increased from 0% to 14% in both groups at 18 weeks, corresponding with the time of sexual maturity. Of the 1,050 eggs cultured from the IBDV+SE-infected group, SE was isolated from 88 shells, five albumens, and two yolks. In contrast, of 1,258 eggs from the SE-infected group, 33 shells and none of the albumens and yolks were positive for SE. All eggs that had SE-positive contents also had SE-positive shells.

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PubMedDate not supplied

Expression of MD infectious bursal disease viral proteins in baculovirus.

Genomic segment A of the variant infectious bursal disease virus (IBDV) strain MD was amplified by reverse transcriptase/polymerase chain reaction and further characterized by baculovirus expression. Three different baculovirus clones were constructed containing the genes encoding VP2, VP2/VP4, and the complete polyprotein cloned into the baculovirus transfer vector pVL1392. Baculovirus recombinants were identified by dot blot hybridization and were plaque purified three times. Baculovirus expression of the recombinants produced IBDV-specific proteins that were comparable in molecular size to native MD IBDV viral proteins VPX (48 kD), VP2 (45 kD), VP3 (32 kD), and VP4 (28 kD) as determined by sodium dodecyl sulfare-polyacrylamide gel electrophoresis and western immunoblot analysis. All three recombinants produced a 48-kD protein that possibly represents VPX, the precursor product of VP2. In addition to the 48-kD protein, the VP2/VP4 recombinant produced an IBDV-specific protein corresponding to the 28-kD VP4. The baculovirus-expressed polyprotein gene produced, in addition to the 48-kD protein, a 32-kD (VP3) IBDV-specific protein and a 29-kD protein that migrated slightly slower than MD VP4. The baculovirus-expressed proteins were used as antigens in an indirect enzyme-linked immunosorbent assay (ELISA). The ELISAs detected antibodies against the variant IBDV strains MD, GLS, and IN and the classic IBDV strains SAL and STC but did not detect antibodies against the variant Del-A and classic IBDV strain BVM or the serotype 2 IBDV strain OH.

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PubMed2004

Infectious bursal disease virus polyprotein expression arrests growth and mitogenic stimulation of B lymphocytes.

Infectious bursal disease virus (IBDV) causes lymphocytolysis and immunosuppression in infected poultry. The IBDV genome encodes a polyprotein VP243 that is post-translationally cleaved by the VP4 protease into the two structural proteins pVP2 and VP3. The objective of the present study was to determine if IBDV polyprotein induced suppression of bursal B lymphocyte growth and their capacity for proliferation. Bursal B cells were examined both for chickens infected with IBDV and for chickens orally inoculated with a DNA construct expressing IBDV VP243 polyprotein. Bursae were collected at 0, 12, 24 and 48 hours after inoculation. Proliferation of bursal B cells (purified AvBu1(+) cells) in response to concanavalin A mitogenic stimulation was significantly suppressed by infection at 1 day old with either the classical STC or variant E strains of IBDV. Oral administration of DNA constructs expressing the IBDV VP243 polyprotein from either the classical STC or variant E strains in the pCR3.1 vector resulted in persistent, moderate levels of construct in the bursa until at least 48 hours after inoculation. The VP243 DNA construct similarly induced suppression of proliferation for bursal lymphocytes independently of the virus infection. Expression of VP243 polyprotein in transiently transfected DT40 B lymphocyte culture also suppressed cell growth and proliferative responses to mitogen stimulation. Polyprotein expression did not affect cell viability and suppression of proliferation probably occurred by means of cell cycle arrest. The expression of the mature viral proteins VP2, VP4 or VP3 did not change the rate of cell proliferation or response of B cell cultures to mitogen. The results suggested that IBDV polyprotein is a mediator of immunosuppression.

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PubMed2001

Rescue of infectious bursal disease virus from mosaic full-length clones composed of serotype I and II cDNA.

Infectious Bursal Disease Virus (IBDV) is the causative agent of one of the most important and wide-spread infectious diseases among commercial chicken flocks. IBDV causes a depletion of B-lymphoid cells in the bursa of Fabricius, inducing immunosuppression, morbidity, or even acute mortality. Because currently used live IBDV vaccines are derivatives from field isolates no serologic discrimination between field isolates and live vaccines can be made. The recently developed reverse genetics techniques for IBDV allows one to generate genetically modified IBDVs which might have altered biological and antigenic properties. Here, we describe the rescue of mosaic serotype I IBDVs, of which the polyprotein encoding region was partly replaced by the corresponding region of a serotype II strain. A mosaic virus, containing the C-terminal part of serotype II VP3 showed only a slightly delayed release of progeny virus compared to unmodified serotype I virus, while maximum viral titers at 25 h post infection were equal. Since serotype specific epitope(s) are present in the C-terminal part of VP3, we were able to discriminate this rescued virus from serotype I and II IBDV strains. These findings make the use of a chimeric VP3 a promising approach to develop an IBDV marker vaccine.

Amino Acid Sequence↗

PubMed2006

The effect of co-administration of DNA carrying chicken interferon-gamma gene on protection of chickens against infectious bursal disease by DNA-mediated vaccination.

The purpose of the present study was to determine whether DNA vaccination by co-administration of DNA coding for chicken interferon-gamma (IFN-gamma) gene and DNA encoding for the VP243 gene of IBDV could enhance immune response and protection efficacy of chickens against challenge by IBDV. Plasmids carrying VP243 gene of IBDV strain variant E (VE) (P/VP243/E) and chicken IFN-gamma gene (P/cIFN-gamma) were constructed, respectively. One-day-old chickens were intramuscularly injected with P/VP243/E, or P/cIFN-gamma, or both once, twice, or three times into the thigh muscle of one leg or the thigh muscles of two separate legs at weekly intervals. Chickens were orally challenged with IBDV strain VE at 3 weeks of age and observed for 10 days. Chickens receiving two plasmids in the same site two times had significantly higher (P<0.05) bursal lesion scores and significantly lower (P<0.05) bursa weight/body weight ratios than those that only received P/VP243/E two or three times. Chickens inoculated with two plasmids separately in the thigh muscles of different legs or P/VP243/E two times had 33-50% protection and those receiving two plasmids in the same sites did not have any protection against IBD. The enzyme-linked immunosorbent assay (ELISA) and virus neutralization (VN) titers to IBDV of chickens in the groups with three doses of P/VP243/E were significantly higher (P<0.05) than those in groups receiving two doses of P/VP243/E or P/VP243/E and P/cIFN-gamma. Chickens protected by DNA vaccination did not have detectable IBDV antigen in the bursae as determined by immunofluorescent antibody assay (IFA). The results indicated that co-administration of plasmid encoding chicken IFN-gamma gene with plasmid encoding a large segment gene of the IBDV did not enhance immune response and protection against challenge by IBDV.

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PubMed2002

The role of T cells in protection by an inactivated infectious bursal disease virus vaccine.

The current belief is that the humoral immune response plays the principal role in defense against virulent infectious bursal disease virus (IBDV). In this study we used a model, in which chickens were compromised in functional T cells by neonatal thymectomy and Cyclosporin A (TxCsA) treatment, to demonstrate the role of T cells in protective immunity against IBDV. We demonstrated that T cells were necessary to achieve full protection against virulent IBDV. When T cell compromised TxCsA-treated chickens were vaccinated with an inactivated IBDV (iIBDV) vaccine, 91% were not protected against IBDV challenge in comparison to T cell-intact chickens, which had a protection rate of 91%. The iIBDV vaccine induced virus neutralizing (VN) and ELISA antibodies, respectively, in 65 and 5% of TxCsA-treated, and in 100 and 58% of T cell-intact birds. These observations provide evidence that the stimulation of T helper cells is needed for the production of protective antibody levels in iIBDV-vaccinated chickens. Passive administration of VN anti-IBDV antibodies inducing a circulating antibody level of log(2)8 in chickens revealed that the levels of antibodies that protected T cell-intact chickens against virulent IBDV challenge were not protective for TxCsA chickens. These results indicated that antibody alone was not adequate in inducing protection against IBDV in chickens and that T cell-involvement was critical for protection. We propose that the inability of iIBDV to protect TxCsA chickens was due to compromised T cell immunity, functional T helper cells and most likely also cytotoxic T cells are needed in iIBDV vaccine protection.

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PubMed2002

Characterization of the antigenic, immunogenic, and pathogenic variation of infectious bursal disease virus due to propagation in different host systems (bursa, embryo, and cell culture). I. Antigenicity and immunogenicity.

In vitro and in ovo virus neutralization assays were conducted to assess the role of different host systems in infectious bursal disease virus (IBDV) antigenic and immunogenic variation. Four different strains, two variant (1084 E and GLS) and two standard (Edgar and STC), were propagated separately in the bursa of Fabricius and embryos, and were compared with cell culture-adapted preparations of the homologous strains. Chicken polyclonal antisera were prepared against each IBDV and neutralizing antibody titres were determined. Normalized IBDV antibody concentrations were used in neutralization assays against homologous and heterologous IBDVs in 10-day-old specific pathogen free embryos. Both antigenic and immunogenic changes occurred in IBDVs evaluated, as evidenced by differences in the ability of normalized antibody to neutralize IBDV propagated in different host systems. Antibody induced by bursal-derived IBDV neutralized all isolates equally well, whereas antibody induced by cell culture-derived virus neutralized bursal-derived IBDV much less effectively.

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PubMed2002

Characterization of the antigenic, immunogenic, and pathogenic variation of infectious bursal disease virus due to propagation in different host systems (bursa, embryo, and cell culture). III. Pathogenicity.

Differences in the relative pathogenicity of variant (1084 E and GLS) and standard (Edgar and STC) infectious bursal disease virus (IBDV) strains were observed after propagation in the bursa of Fabricius, embryos, or cell cultures. Bursa-derived IBDV induced the most severe lesions in the bursa of Fabricius when compared with strains propagated in embryos or cell cultures. Embryo-derived IBDV induced moderate gross bursal lesions, whereas cell culture-derived IBDV did not damage the bursa grossly. A high frequency of virus re-isolations was obtained from bursal, spleen, and thymic samples collected from birds inoculated with bursa-derived or embryo-derived IBDV. Virus re-isolation occurred much less frequently from birds inoculated with cell culture-adapted IBDV. Serological evaluations demonstrated that bursa-derived IBDV strains induced a higher neutralizing antibody response than did embryo-derived or cell culture-derived strains. These results document that the relative pathogenicity and immunogenicity of IBDV is reduced following propagation in embryos or cell cultures.

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PubMed2000

Characteristics of bursal T lymphocytes induced by infectious bursal disease virus.

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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