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PubMedDate not supplied

Sequence comparisons of a highly virulent infectious bursal disease virus prevalent in Japan.

Variable cDNA regions in the VP2 gene of five highly virulent infectious bursal disease viruses (IBDVs) isolated in Japan were amplified by polymerase chain reaction (PCR) and sequenced. The nucleotide sequences of five highly virulent IBDVs were identical. Comparisons of the nucleotide and the deduced amino acid sequences with those of other strains of IBDV indicated that Japanese highly virulent IBDV is different from all other strains of IBDV that were compared. The number of amino acids that differed between strains (substitution score) showed that highly virulent IBDV is more closely related to European virulent strain 52/70 than to Japanese conventional strains. These results strongly suggest that a single strain of highly virulent IBDV that might have originated from a European strain is prevalent in Japan.

Amino Acid Sequence↗

PubMedDate not supplied

Restriction fragment length polymorphisms in the VP2 gene of infectious bursal disease viruses.

Infectious bursal disease viruses (IBDVs) were examined for restriction fragment length polymorphisms in a fraction of the VP2 gene with the use of the reverse transcriptase/polymerase chain reaction-restriction fragment length polymorphism (RT/PCR-RFLP) assay. The restriction enzymes BstNI and Mbol were used to obtain RFLP results. A third enzyme, StyI, was tested, but its utility for differentiation of IBDV strains was limited. Thirteen vaccine viruses and five IBDV strains that were previously characterized were placed into five molecular groups. Two groups contained viruses described as being classic strains, and two groups contained viruses described as being variant strains. The fifth group contained both classic and variant strains. The RFLP observed for the serotype 2 IBDV strain OH was unlike any of the RFLPs observed in viruses in the five molecular groups. Seven IBDV strains from commercially reared chickens in the United States, Mexico, Puerto Rico, and Thailand were tested in the RT/PCR-RFLP assay to determine if they were similar to the commercial IBDV vaccine strains tested. These viruses were selected because they were associated with lesions in the bursa of chickens that should have been protected by maternal antibodies or active immunity. Each of the viruses tested contained a unique RFLP compared with the IBDV strains and vaccine viruses examined in this study and, thus, did not fit into any of the five molecular groups. These viruses also were distinguishable from each other.

Animals↗

PubMedDate not supplied

Genetic heterogeneity in the VP2 gene of infectious bursal disease viruses detected in commercially reared chickens.

The genetic heterogeneity of infectious bursal disease virus (IBDV) vaccine strains was compared with IBDV detected in bursa tissue of commercially reared chickens. The vaccine strains tested represented classic viruses from the United States, South Africa, England, and France plus variant viruses from the United States. Bursa tissue samples used for the detection of IBDV from commercially reared chickens were from the United States. Genetic heterogeneity was examined using restriction fragment length polymorphisms (RFLP) of a 743-bp fragment of the VP2 gene that was amplified using reverse transcriptase/polymerase chain reaction (RT/PCR). The RT/PCR products were digested using restriction enzymes BstNI and MboI. On the basis of RFLP profiles, viruses were placed into molecular groups. Thirty-eight vaccine and laboratory strains of IBDV were placed into five molecular groups. Groups 1 and 2 contained variant viruses, groups 3 and 4 contained classic viruses, and group 5 contained Lukert/Edgar strain classic viruses. In contrast to these five molecular groups, 22 molecular groups were observed for 70 IBDV-positive samples from U.S. chicken flocks. Twenty-two of the 70 IBDV-positive samples were placed into molecular groups 1 (2 samples), 2 (18 samples), and 5 (2 samples). Nineteen new RFLP profiles that did not match the five molecular groups observed for vaccine strains were detected. No viruses were observed to have RFLP profiles like molecular groups 3 and 4 observed in the vaccine strains. The genetic heterogeneity was greater among IBDV strains circulating in commercially reared poultry compared with vaccine strains of the virus.

Animals↗

PubMedDate not supplied

Simplified sample processing combined with a sensitive nested polymerase chain reaction assay for detection of infectious bursal disease virus in the bursa of Fabricus.

A rapid and sensitive protocol for the detection and amplification of infectious bursal disease virus (IBDV) RNA in the bursa of Fabricius was developed. By digestion with proteinase K and subsequent extraction with phenol and chloroform, IBDV RNA was efficiently released from a single bursa. IBDV RNA extraction time was shortened to 4 hr, compared with 24 hr with the traditional method, and only one bursa was needed instead of five. This more simplified procedure resulted in a significant reduction in costs due to less labor and the reduction in expensive chemicals and reagents. Four primers were selected from the sequence of a hypervariable region in VP2 genes. For the amplification of genomic IBDV RNA, the product (643 bp) of reverse transcriptase-polymerase chain reaction (RT-PCR) was reamplified and double checked by a nested PCR amplifying a 491-bp cDNA. The sensitivity of nested PCR was at least 100 times greater than RT-PCR as determined by dilution of the bursal homogenate. The fidelity of the nested PCR product was confirmed by Southern blotting, demonstrating specificity to the VP2 gene of IBDV. The simplified sample processing, shortened procedure time, and technical ease of this nested PCR render it more suitable for implementation in routine RT-PCR with restriction fragment length polymorphism testing for the detection and differentiation of IBDV RNA, especially for studies of IBDV infections of individual chickens.

Animals↗

PubMed1998

Alteration of chicken heterophil and macrophage functions by the infectious bursal disease virus.

The effects of the infectious bursal disease virus (IBDV) on chicken heterophils and macrophages are reported. Short-term incubation of IBDV with heterophils causes an activation of cellular oxidative burst, a decrease in phagocytosis and cellular migration, and an increase in cellular adherence to the IBDV-infected chicken embryo fibroblasts. Under electron microscopic examination, heterophils show condensed chromatin and packets of intact granules, either free or being phagocytized by macrophages, indicating that the heterophils are undergoing apoptosis. The HD-11 cells, a virus-transformed macrophage cell, after 1-2 h of infection by IBDV in vitro, become less responsive of chemoattractant and less capable of performing phagocytosis. After a longer period of infection, IBDV is able to multiply in the HD-11 cells, and starts to cause cells to undergo apoptosis. This IBDV-induced alteration in heterophil and macrophage functions and the death of these phagocytic cells may play a role in the subsequent immunosuppression in the affected chickens.

Animals↗

PubMed1997

Sequence and phylogenetic analyses of highly virulent infectious bursal disease virus.

The nucleotide sequences of the genome segments A and B encoding the precursor polyprotein (NH2-VP2-VP4-VP3-COOH) and VP1 were determined for a highly virulent strain of infectious bursal disease virus (IBDV). The precursor polyprotein and VP1 coding regions of highly virulent OKYM strain consisted of 3039 nucleotides (1012 deduced amino acids) and 2640 nucleotides (879 deduced amino acids), respectively. Comparison of the deduced amino acid sequences of the highly virulent IBDV (HV-IBDV) with other serotype 1 and 2 sequences revealed 17 amino acid residues which were conserved only in the HV-IBDV. Among the 17 unique amino acid differences, 8 were in VP1, 4 were in VP2, 3 were in VP3 and 2 were in VP4. Although it is impossible to predict the effect of the unique amino acid residues without detailed knowledge of the three-dimensional structure and function of the proteins, they could affect the virulence of HV-IBDV. Alignment of the nucleic acid sequences of precursor polyprotein, VP1, VP2, VP3 and VP4 coding regions followed by distance analysis allowed the generation of phylogenetic trees. The same tree topology was obtained for the nucleotide sequence of precursor polyprotein, VP2, VP3 and VP4. On the other hand, the tree topology of VP1 was quite different from that obtained for the nucleotide sequence of precursor polyprotein, VP2, VP3 and VP4. These findings indicate that not a genetic recombination but a genetic reassortment may play an important role in the emergence of HV-IBDV.

Amino Acid Sequence↗

PubMed1996

Coding sequences of both genome segments of a European 'very virulent' infectious bursal disease virus.

The sequences of segment A (encoding the VP2-VP4-VP3 polyprotein and VP5) and segment B (encoding VP1) of a recent, 'very virulent' (VV) European isolate (UK661) of infectious bursal disease virus (IBDV), a birnavirus, have been determined. There are 26 to 36 amino acid substitutions compared to any other type I IBDV within the segment A polyprotein (of these, 15 are unique) and about 50 substitutions within VP1 (of which 16 are unique). There is more variation compared to classical and antigenic variant viruses, of both virulent and attenuated phenotype, in VP1, VP3 and VP4 than in VP2, even though the latter has previously been identified as the most variable protein between different strains of type I IBDV. In VP3 and VP4, UK661 is the most diverged type I IBDV. Thus the origin of the virus is unclear. It is possible that strong functional constraints have preferentially maintained the primary structure of VP2, though the possibility of recombination cannot be excluded. There are no clear candidate mutations to account for the enhanced virulence of the VV IBDV. Polymerase motifs are well conserved in VP1 but there is an amino acid substitution next to the predicted active-site serine of the viral protease (VP4). In addition, there is a conservative substitution close to the postulated VP2-VP4 cleavage site. It is also now apparent that sequences of IBDV segment B (the segment encoding the RNA polymerase) do not group according to serotype (specified by the capsid proteins encoded on segment A), indicating that segment reassortment has occurred.

Amino Acid Sequence↗

PubMed2004

Development of a multiplex PCR for detection of avian adenovirus, avian reovirus, infectious bursal disease virus, and chicken anemia virus.

A multiplex polymerase chain reaction (mPCR) was developed and optimized for the simultaneous detection and differentiation of avian reovirus (ARV), avian adenovirus group I (AAV-I), infectious bursal disease virus (IBDV), and chicken anemia virus (CAV). Four sets of specific oligonucleotide primers were used in this test for ARV, AAV-I, IBDV, and CAV. The mPCR DNA products were visualized by gel electrophoresis and consisted of fragments of 365 bp for IBDV, 421 bp for AAV-I, 532 bp for ARV, and 676 bp for CAV. The mPCR assay developed in this study was found to be sensitive and specific. Detection of PCR-amplified DNA products was 100 pg for both CAV and IBDV, and 10pg for both ARV and AAV-I and this mPCR did not amplify nucleic acids from the other avian pathogens tested. The mPCR demonstrated similar sensitivity in tests using experimental fecal cloacal swab specimens that were spiked with ARV, AAV-1, IBDV, and CAV, and taken from specific pathogen free (SPF) chickens. This mPCR detected and differentiated various combinations of RNA/DNA templates from ARV, AAV-I, CAV, and IBDV without reduction of amplification from feces.

Animals↗

PubMed2005

Development of recombinant VP2 vaccine for the prevention of infectious bursal disease of chickens.

The objective of the present study was to investigate the feasibility of a subunit vaccine and a live bacteria vaccine to protect chickens against infectious bursal disease virus (IBDV) infection. The gene for VP2 of a new wild-type very virulent IBDV (vvIBDV) strain was cloned into an Escherichia coli expression system. Following expression, the recombinant VP2 and the induced expression bacteria were used to vaccinate chickens against virulent IBDV (vIBDV). Three weeks after the vaccination, chickens were inoculated with IBDV strain BC 6/85 by intranasal route or eyedrop route, prior to challenge anti-IBDV serum antibody was detected by AGP. All chickens vaccinated with recombinant VP2 could be detected anti-IBDV antibody. The subunit vaccine of recombinant VP2 conferred protection for 90--100% chickens, live bacteria vaccine of recombinant VP2 conferred protection for 85.7% chickens. The results indicate that E. coli BL 21/pET 28 a-VP2 could be used to develop recombinant VP2 vaccine against infectious bursal disease in chickens.

Administration, Intranasal↗

PubMed2004

Enhancement of the immunogenicity of DNA vaccine against infectious bursal disease virus by co-delivery with plasmid encoding chicken interleukin 2.

The immunoregulatory activity of a nonmammalian interleukin 2 (IL-2), chicken IL-2 (chIL-2), was investigated using a DNA vaccine against infectious bursal disease virus (IBDV) as a model. Coadministration of a plasmid encoding the VP2 gene of IBDV (pCI-VP2) and a plasmid encoding chicken IL-2 gene (pCI-chIL-2) enhances bursal protection against both the homologous IBDV strain ZJ2000 and the heterologous strain BC6/85 compared to administration of pCI-VP2 alone. Vaccination with pCI-VP2 alone induces low bursal protection against ZJ2000 and only protects chickens from clinical outbreaks and mortality, but not from bursal damage caused by BC6/85. Co-administration of the plasmid encoding the polyprotein gene of IBDV (pCI-VP2/4/3) and pCI-chIL-2 provides complete protection (15/15) against ZJ2000 and satisfactory protection (13/15) against BC6/85. In contrast, only 10 out of 15 chickens and 6 out of 15 chickens were protected against ZJ2000 and BC6/85, respectively, using the pCI-VP2/4/3 vaccination alone. A significant increase in the IBDV-specific neutralizing antibody response was also observed in chickens that received pCI-VP2/4/3 plus pCI-chIL-2 as compared with those that received the pCI-VP2/4/3 vaccination alone. By administrating different amounts of plasmid DNA, we confirmed that the pCI-chIL-2, but not the backbone plasmid pCI, contributes to increased immunoprotection of DNA vaccine against IBDV. These results strongly indicate that the efficacy of avian DNA vaccine can be modulated by co-administration of a plasmid encoding chIL-2.

Adjuvants, Immunologic↗

PubMedDate not supplied

Infectious bursal disease virus of chickens: pathogenesis and immunosuppression.

Infectious bursal disease virus (IBDV) is an important immunosuppressive virus of chickens. The virus is ubiquitous and, under natural conditions, chickens acquire infection by the oral route. IgM+ cells serve as targets for the virus. The most extensive virus replication takes place in the bursa of Fabricius. The acute phase of the disease lasts for about 7-10 days. Within this phase, bursal follicles are depleted of B cells and the bursa becomes atrophic. Abundant viral antigen can be detected in the bursal follicles and other peripheral lymphoid organs such as the cecal tonsils and spleen. CD4(+) and CD8(+) T cells accumulate at and near the site of virus replication. The virus-induced bursal T cells are activated, exhibit upregulation of cytokine genes, proliferate in response to in vitro stimulation with IBDV and have suppressive properties. Chickens may die during the acute phase of the disease although IBDV induced mortality is highly variable and depends, among other factors, upon the virulence of the virus strain. Chickens that survive the acute disease clear the virus and recover from its pathologic effects. Bursal follicles are repopulated with IgM(+) B cells. Clinical and subclinical infection with IBDV may cause immunosuppression. Both humoral and cellular immune responses are compromised. Inhibition of the humoral immunity is attributed to the destruction of immunoglobulin-producing cells by the virus. Other mechanisms such as altered antigen-presenting and helper T cell functions may also be involved. Infection with IBDV causes a transient inhibition of the in vitro proliferative response of T cells to mitogens. This inhibition is mediated by macrophages which are activated in virus-exposed chickens and exhibit a marked enhancement of expression of a number of cytokine genes. We speculate that T cell cytokines such as interferon (IFN)-gamma may stimulate macrophages to produce nitric oxide (NO) and other cytokines with anti-proliferative activity. Additional studies are needed to identify the possible direct immunosuppressive effect of IBDV on T cells and their functions. Studies are also needed to examine effects of the virus on innate immunity. Earlier data indicate that the virus did not affect normal natural killer (NK) cell levels in chickens.

Animals↗

PubMed1997

Quantitative competitive polymerase chain reaction for detection and quantification of infectious bursal disease virus cDNA and RNA.

A polymerase chain reaction (PCR)-based method to measure complementary DNA (cDNA) and RNA levels of infectious bursal disease virus (IBDV) was developed. Quantification was achieved by quantitative competitive PCR (QC-PCR) amplification. A competitor, a deletion mutant of the wild type IBDV cDNA, was 10-fold serially diluted and co-amplified with IBDV cDNA after being reversely transcribed from the viral RNA. After agarose gel electrophoresis, staining, and densitometric scanning, the bands on the digitized images were analyzed and quantified by computer-assisted image analysis. Complementary DNA of standard, as well as variant strains, of serotype 1 IBDV was detected and quantified using the same QC-PCR procedures. The assay could measure IBDV cDNA levels ranging from 1 microgram to 45 fg and RNA levels ranging from 9 micrograms to 45 fg. The results indicated that QC-PCR is sensitive, easy to perform, and suitable for routine quantitation of IBDV cDNA or RNA levels.

Animals↗

PubMed2000

Measuring infectious bursal disease virus RNA in blood by multiplex real-time quantitative RT-PCR.

A quantitative reverse transcription polymerase chain reaction (RT-PCR) protocol for assessing infectious bursal disease virus (IBDV) RNA levels in blood was developed using the ABI PRISM 7700 Sequence Detection System coupled with TaqMan chemistry. To control for variations in sampling and processing between samples 28S rRNA was co-amplified in a multiplex reaction and used to quantify total RNA. Relative quantification and standardisation was achieved using a log10 dilution series of RNA extracted from IBDV stock. A linear relationship was observed between input RNA and cycle threshold values (C(T)) over 5 log10 dilutions for the IBDV-specific product and 6 log10 dilutions for the 28S rRNA-specific product. As a test of the assay it was used to determine whether differences in susceptibility to IBDV observed between inbred lines of chickens could be detected at the level of viral load in the blood. Viral RNA levels peaked 2 days post-infection when there was significantly less viral RNA in the blood of resistant line 6(1) chickens compared with the more susceptible Brown Leghorns (P = 0.01). These results demonstrate that the course of IBDV infection can be monitored by quantifying IBDV RNA extracted from blood of infected chickens using TaqMan technology.

Animals↗

PubMed2004

Base usage and dinucleotide frequency of infectious bursal disease virus.

Base usage and dinucleotide frequency have been extensively studied in many eukaryotic organisms and bacteria, but not for viruses. In this paper, a comprehensive analysis of these aspects for infectious bursal disease virus (IBDV) was presented. The analysis of base usage indicated that all of the IBDV genes possess equivalent overall nucleotide distributions. However when the base usage at each codon positions was analysed by using cluster analysis, the VP5 open reading frame (ORF) formed a different cluster isolated from the other genes. The unusual base usage of VP5 ORF may indicate that the gene was originated by the virus "overprinting strategy", a strategy in which virus may create novel gene by utilizing the unused reading frames of its existing genes. Meanwhile, the GC content of the IBDV genes and the chicken's coding sequences was comparable; suggesting the virus imitation of the host to increase its translational efficiency. The analysis of dinucleotide frequency indicated that IBDV genome had dinucleotide bias: the frequencies of CpG and TpA were lower and the TpG was higher than the expected. Classical methylation pathway, a process where CpG converted to TpG, may explain the significant correlation between the CpG deficiency and TpG abundance. "Principal component analysis of the dinucleotide frequencies" (DF-PCA) was used to analyse the overall dinucleotide frequencies of IBDV genome. DF-PCA on the hypervariable region and polyprotein (VPX-VP4-VP3) gene showed that the very virulent IBDV (vvIBDV) was segregated from other strains; which meant vvIBDV had a unique dinucleotide pattern. In summary, the study of base usage and dinucleotide frequency had unravelled many overlooked genomic properties of the virus.

Animals↗

PubMed1999

Persistent infection with chicken anaemia virus and some effects of highly virulent infectious bursal disease virus infection on its persistency.

Chicken anaemia virus (CAV) infectivity and the effect of highly virulent infectious bursal disease virus (hv IBDV) infection on CAV's infectivity were examined in chickens inoculated with CAV or inoculated dually with CAV and hv IBDV. Five chickens inoculated dually with hv IBDV at 35 days old and then with CAV at 40 days old exhibited no clinical signs of disease, but showed atrophic bursae of Fabricius when necropsied 4 weeks later. Upon examining the chickens at 7 days postinoculation (dpi) with CAV, it was found that hv IBDV infection had inhibited production of virus neutralising (VN) antibody to CAV, and that it was possible to recover CAV from plasma of these chickens. Although VN antibody to CAV appeared after 14 dpi, CAV was recovered from blood cells (BC s) at high titres ranging from 10(2.5)to 10(5.5)TCID(50)/0.1 ml, 7 to 28 dpi in IBDV -induced immunosuppressed chickens. In addition, CAV was sporadically recovered, using rectal swabs, from the dually inoculated chickens at low titers, ranging from 10(1.0)to 10(2. 0)TCID(50)/0.1 ml). In contrast, although CAV was recovered from BC s in most of the chickens inoculated with CAV alone, the titers were lower (10(1.0)to 10(2.5)TCID(50)/0.1 ml). No CAV was detected from the rectal swabs of these chickens. The results of virus recovery were confirmed by polymerase chain reaction. This study first examined the persistency of CAV in BC s and the effective enhancement of primary CAV infection as a result of immunosuppression caused by hv IBDV infection.

Anemia↗

PubMed1999

Development of an experimental model of bacterial chondronecrosis with osteomyelitis in broilers following exposure to Staphylococcus aureus by aerosol, and inoculation with chicken anaemia and infectious bursal disease viruses.

A series of experiments was designed in an attempt to reproduce bacterial chondronecrosis with osteomyelitis in broiler chickens using a natural route of infection. Birds in isolators were exposed to a suspension of Staphylococcus aureus by aerosol or exposed to S. aureus and subsequently inoculated with chicken anaemia virus (CAV) alone, or with CAV and infectious bursal disease virus (IBDV). Subsequently, S. aureus was recovered and bacterial chondronecrosis with osteomyelitis was diagnosed, by histology, in the proximal end of the femur and/or tibiotarsus of lame birds exposed to S. aureus with and without CAV and IBDV infections. Birds fed 60% of the recommended feed intake for the breed developed a lower incidence of S. aureus infection and/or bacterial chondronecrosis (P < 0.05) than birds fed 100% of the recommended intake. A significantly lower incidence of S. aureus was recovered (P < 0.05) in birds simultaneously exposed to S. aureus and inoculated with CAV and IBDV at day 21, than in birds exposed to S. aureus at day 10, and inoculated with CAV and IBDV at day 21. With the exception of birds exposed to S. aureus at 1 day old, a higher incidence of bacterial chondronecrosis was diagnosed in birds exposed to S. aureus and inoculated with CAV and IBDV than in birds exposed to S. aureus alone. It is hypothesised that inoculation with CAV and IBDV at day 21 enhanced the development of bacterial chondronecrosis in birds exposed to S. aureus at day 10 and fed 100% of the recommended feed intake or ad libitum.

Journal Article↗

PubMed2006

In vitro expression and monoclonal antibody of RNA-dependent RNA polymerase for infectious bursal disease virus.

VP1, the RNA-dependent RNA polymerase of infectious bursal disease virus (IBDV), has been suggested to play an essential role in the replication and translation of viral RNAs. In this study, we first expressed the complete VP1 protein gene in Escherichia coli (E. coli), and then the produced polyclonal antibody and four monoclonal antibodies (mAbs) to recombinant VP1 protein (rVP1) were shown to bind the IBDV particles in chicken embryo fibroblast and Vero cells. The epitopic analysis showed that mAbs 1D4 and 3C7 recognized respectively two distinct antigenic epitopes on the rVP1 protein, but two pair of mAbs 1A2/2A12 and 1E1/1H3 potentially recognized another two topologically related epitopes. Immunocytochemical stainings showed that VP1 protein formed irregularly shaped particles in the cytoplasm of the IBDV-infected cells. These results demonstrated that the mAbs to rVP1 protein could bind the epitopes of IBDV particles, indicating that the rVP1 protein expressed in E. coli was suitable for producing the mAb to VP1 protein of IBDV, and that the cytoplasm could be the crucial site for viral genome replication of IBDV.

Animals↗

PubMed2002

Major histocompatibility complex-linked immune response of young chickens vaccinated with an attenuated live infectious bursal disease virus vaccine followed by an infection.

The influence of the MHC on infectious bursal disease virus (IBDV) vaccine response in chickens was investigated in three different chicken lines containing four different MHC haplotypes. Two MHC haplotypes were present in all three lines with one haplotype (B19) shared between the lines. Line 1 further contains the BW1 haplotype isolated from a Red Jungle Fowl. Line 131 further contains the B131 haplotype isolated from a meat-type chicken. Finally, Line 21 further contains the international B21 haplotype. The chickens were vaccinated with live attenuated commercial IBDV vaccine at 3 wk of age, followed by a challenge with virulent IBDV at 6 wk of age. In this study, we found a notable MHC haplotype effect on the specific antibody response against IBDV, as measured by ELISA. The BW1 haplotype was found to have a significantly higher serum antibody titer against IBDV (7,872) than haplotypes B19 (mean 5,243), B21 (5,570), and B131 (5,333) at 8 d postinfection. However, a virus-neutralizing antibody test did not reflect this result. Nevertheless, the MHC haplotype-associated protective immunity was further supported by the bursa of Fabricius (bursa) recovery from the disease, as measured by histological scorings of the bursa. Chickens carrying the BW1 haplotype had a significantly lower bursa lesion score (1.7) than the haplotypes B19 (mean 3.8), B21 (3.6), and B131 (4.3) 8 d postinfection. Furthermore, multiple line effects were found in other variables when comparing Day 6 with Day 8. Body weight, relative weights of the bursa and the spleen, percentage and relative number of MHC II molecules on MHC II-positive lymphocytes, percentage and relative number of CD4 molecules on CD4-positive lymphocytes, and the specific antibody response all differed significantly among lines. Line 1, with Red Jungle Fowl genes, was clearly differentiated from the other two investigated lines. These results suggest an MHC II restricted T-cell dependent secondary antibody response against IBDV.

Animals↗