Chicken Trachea Research Articles

Molecular cloning and characterization of a novel chicken gene named grni

The full-length cDNA sequence of a novel expressed sequence tag (GenBank accession No. HQ184338) that was differentially expressed during Newcastle disease virus (NDV) infection in chickens was cloned from the chicken spleen by a rapid amplification of cDNA ends assay. This gene was further analyzed using bioinformatic methods and named grni. The full-length cDNA sequence was 1698 bp without introns, locating between 104,691,934 and 104,693,618 in galGal4 on chromosome 2. The open reading frame (ORF) contained 261 bp and encoded a deduced protein of 86 amino acid residues. Furthermore, the encoded protein contained two transmembrane regions without signal peptides, indicating that this protein is located in the mitochondrial membrane. Moreover, its homologous protein was not identified. Real-time polymerase chain reaction was used to detect the dynamic mRNA expression of this gene in the spleen, thymus, bursa of Fabricius, and trachea of NDV-infected chickens. Results suggested that the gene was involved in the transcriptional response of chicken to NDV infection. To obtain a fusion protein and prepare rabbit anti-serum, the predicted ORF of this gene was expressed in Escherichia coli. The expression of this gene at the protein level was further confirmed in the spleen, thymus, and bursa of Fabricius of NDV-infected chickens using Western blot analysis. In conclusion, a novel protein-coding gene named grni was successfully cloned and identified in chickens. Furthermore, this gene was found to be involved in the response of chickens to NDV infection.

The expression dynamics of IL-17 and Th17 response relative cytokines in the trachea and spleen of chickens after infection with Cryptosporidium baileyi.

BackgroundCryptosporidium baileyi is the dominant Cryptosporidium species in birds causing emerging health problems in the poultry industry, and is also a model to study the biology of Cryptosporidium spp.. IL-17 (also called IL-17A) is a hallmark pro-inflammatory cytokine of Th17 cells that plays an important role in several human autoimmune diseases and microbial infection disease of many animals, and it may play a role in Cryptosporidium infection.MethodsThe present study examined the mRNA level of IL-17 and Th17 response relative cytokines in the trachea and spleen of C. baileyi-infected chickens at different time points using real-time quantitative PCR (qPCR).ResultsAll examined cytokines in the trachea were up-regulated in the infected chickens compared with the uninfected control during C. baileyi infection. Significant increased IL-17 mRNA level in the trachea was observed as early as 12 h post infection (pi), peaking at 24 h pi and 10 d pi, and declining thereafter. The transcription levels of IL-17 and Th17 response relative cytokines in spleen were also significantly increased at different time points during the infection.ConclusionsIL-17 was indicated to participate in the induction of inflammation during infection of some intracellular protozoan parasites. The results in the present study suggest that IL-17 may play a role in immunity against Cryptosporidium infection, and provide basic information for determining the role of Th17 cell in Cryptosporidium infection.

Induction of innate immune response following infectious bronchitis corona virus infection in the respiratory tract of chickens

Infectious bronchitis virus (IBV) replicates in the epithelial cells of trachea and lungs of chicken, however the mechanism of generation of innate immune response against IBV infection in these tissues has not been fully characterized. Our objective was to study innate responses induced early following IBV infection in chickens. Initiation of the transcription of selected innate immune genes such as TLR3, TLR7, MyD88, IL-1β and IFN-β, as well as recruitment of macrophages, were evident following an initial down regulation of some of the observed genes (TLR3, IL-1β, and IFN-γ) in trachea and lung. This initial down-regulation followed by the induction of innate immune response to IBV infection appears to be inadequate for the control of IBV genome accumulation and consequent histopathological changes in these tissues. Potential induction of innate immunity before infection occurs may be necessary to reduce the consequences since vaccine induced immunity is slow to develop.

Contributions of the S2 spike ectodomain to attachment and host range of infectious bronchitis virus

The spike protein is the major viral attachment protein of the avian coronavirus infectious bronchitis virus (IBV) and ultimately determines viral tropism. The S1 subunit of the spike is assumed to be required for virus attachment. However, we have previously shown that this domain of the embryo- and cell culture adapted Beaudette strain, in contrast to that of the virulent M41 strain, is not sufficient for binding to chicken trachea (Wickramasinghe et al., 2011). In the present study, we demonstrated that the lack of binding of Beaudette S1 was not due to absence of virus receptors on this tissue nor due to the production of S1 from mammalian cells, as S1 proteins expressed from chicken cells also lacked the ability to bind IBV-susceptible embryonic tissue. Subsequently, we addressed the contribution of the S2 subunit of the spike in IBV attachment. Recombinant IBV Beaudette spike ectodomains, comprising the entire S1 domain and the S2 ectodomain, were expressed and analyzed for binding to susceptible embryonic chorio-allantoic membrane (CAM) in our previously developed spike histochemistry assay. We observed that extension of the S1 domain with the S2 subunit of the Beaudette spike was sufficient to gain binding to CAM. A previously suggested heparin sulfate binding site in Beaudette S2 was not required for the observed binding to CAM, while sialic acids on the host tissues were essential for the attachment. To further elucidate the role of S2 the spike ectodomains of virulent IBV M41 and chimeras of M41 and Beaudette were analyzed for their binding to CAM, chicken trachea and mammalian cell lines. While the M41 spike ectodomain showed increased attachment to both CAM and chicken trachea, no binding to mammalian cells was observed. In contrast, Beaudette spike ectodomain had relatively weak ability to bind to chicken trachea, but displayed marked extended host range to mammalian cells. Binding patterns of chimeric spike ectodomains to these tissues and cells indicate that S2 subunits most likely do not contain an additional independent receptor-binding site. Rather, the interplay between S1 and S2 subunits of spikes from the same viral origin might finally determine the avidity and specificity of virus attachment and thus viral host range.

Dynamic distribution and tissue tropism of infectious laryngotracheitis virus in experimentally infected chickens

Infectious laryngotracheitis (ILT), caused by infectious laryngotracheitis virus (ILTV), is an Office International des Epizooties (OIE) notifiable disease. However, we have not clearly understood the dynamic distribution, tissue tropism, pathogenesis, and replication of ILTV in chickens. In this report, we investigated the dynamic distribution and tissue tropism of the virus in internal organs of experimentally infected chickens using quantitative real-time polymerase chain reaction (qPCR) and a histopathological test. The study showed that ILTV could be clearly detected in eight internal organs (throat, trachea, lung, cecum, kidney, pancreas, thymus and esophagus) of infected chickens, whereas the virus was difficult to detect in heart, spleen, proventriculus, liver, brain and bursa. Meanwhile, the thymidine kinase (TK) gene levels in eight internal organs increased from 3 days to 5 days postinfection, and then decreased from 6 days to 8 days postinfection. The log copy number of ILTV progressively increased over 3 days, which corresponds to the clinical score and the result of the histopathological test. The results provide a foundation for further clarification of the pathogenic mechanism of ILTV in internal organs and indicate that throat, lung, trachea, cecum, kidney, pancreas and esophagus may be preferred sites of acute infection, suggesting that the tissue tropism and distribution of ILTV is very broad.

Qualitative and quantitative analyses of influenza virus receptors in trachea and lung tissues of humans, mice, chickens and ducks

To accurately determine the expression and distribution patterns of two influenza virus receptors (SAα2,3-gal and SAα2,6-gal) in trachea and lung tissues of humans, mice, chickens and ducks, we analyzed lectin immunofluorescence stainings of various tissue sections qualitatively and quantitatively. Results from the qualitative analysis showed that both influenza virus receptors were expressed in lung tissues of humans, mice, chickens and ducks as well as trachea tissues of mice and ducks. However, SAα2,6-gal receptor was expressed only in the human trachea tissue and SAα2,3-gal receptor was expressed only in the chicken trachea tissue. Results from the quantitative analysis demonstrated that both receptors were expressed in trachea tissues of human and mouse, as well as in lung tissues of humans, chickens and ducks. Meanwhile, our results also showed that the expression and distribution of influenza virus receptors in the same tissue were not always uniform, indicating that their distribution and expression in various tissues are not simply the distinction between the presence or absence of receptors, but rather the difference in the amount of expressed receptors.

Pathological study on the upper respiratory tract infection of chickens and isolation, identification of causal bacteria

The proportional occurrence of bacteria and pathological lesions in the nasal sinuses and trachea of dead chickens were determined during 2008-2009. Nasal sinus and tracheal swabs from 50 dead birds were collected in sterile nutrient broth. The histopathological samples were collected in 10% neutral buffered formalin and studied with light microscope. The isolation and identification of bacteria were performed by culture, staining and biochemical tests. The proportional occurrence of bacteria in trachea (n = 50) and nasal sinuses (n = 50) of dead chickens was Klebsiella sp. (6.0%), Escherichia coli (38.8%), Pasteurella sp. (8.6%), Bacillus sp. (5.2%) and Staphylococcus sp. (41.4%). Congested trachea (n=3) and mucus-filled sinuses (n = 3) of dead chickens were studied for histopathology. Microscopically, rhinitis was characterized by infiltration of macrophages, lymphocytes and few neutrophils. The epithelium of nasal passage revealed pyknotic nucleus with disruption of epithelium. There was sinusitis with purulent and necrotic changes around the nasal sinus. The nasal sinuses were infiltrated with macrophages, lymphocytes and few plasma cells. The mucosal layer of the nasal turbinates showed pus and necrosis. There was disruption of different mucous glands with accumulation of macrophages, lymphocytes and plasma cells in the submucosa.DOI: http://dx.doi.org/10.3329/bvet.v28i2.10677 Bangl. vet. 2011. Vol. 28, No. 2, 60 – 69

Qualitative and quantitative analyses of influenza virus receptors in trachea and lung tissues of human, mouse, chicken and duck

To determine precisely the expression and distribution patterns of two influenza virus receptors(SAα2,3-gal and SAα2,6-gal) in trachea and lung tissues of human,mouse,chicken and duck,we analyzed lectin immunofluorescence stainings of various tissue sections qualitatively and quantitatively.Results from the qualitative analysis showed that both influenza virus receptors were expressed in lung tissues of human,mouse,chicken and duck as well as trachea tissues of mouse and duck;however,SAα2,6-gal receptor was expressed only in the human trachea tissue and SAα2,3-gal receptor was expressed only in the chicken trachea tissue.Results from the quantitative analysis demonstrated that both receptors were expressed in trachea tissues of human and mouse,as well as in lung tissues of human,chicken and duck.Meanwhile,our results also showed that the expression and distribution of influenza virus receptors in the same tissue were not always uniform,indicating that their distribution and expression in various tissues are not simply the distinction between the presence or absence of receptors,but rather the difference in the amount of expressed receptors.

Proteomics analysis of differentially expressed proteins in chicken trachea and kidney after infection with the highly virulent and attenuated coronavirus infectious bronchitis virus in vivo

BackgroundInfectious bronchitis virus (IBV) is first to be discovered coronavirus which is probably endemic in all regions with intensive impact on poultry production. In this study, we used two-dimensional gel electrophoresis (2-DE) and two-dimensional fluorescence difference gel electrophoresis (2-DIGE), coupled with matrix-assisted laser desorption/ionization time-of-flight tandem mass spectrometry (MALDI-TOF/TOF-MS), to explore the global proteome profiles of trachea and kidney tissues from chicken at different stages infected in vivo with the highly virulent ck/CH/LDL/97I P5 strain of infectious bronchitis virus (IBV) and the embryo-passaged, attenuated ck/CH/LDL/97I P115 strain.ResultsFifty-eight differentially expressed proteins were identified. Results demonstrated that some proteins which had functions in cytoskeleton organization, anti-oxidative stress, and stress response, showed different change patterns in abundance from chicken infected with the highly virulent ck/CH/LDL/97I P5 strain and those given the embryo-passaged, attenuated P115 stain. In addition, the dynamic transcriptional alterations of 12 selected proteins were analyzed by the real-time RT-PCR, and western blot analysis confirmed the change in abundance of heat shock proteins (HSP) beta-1, annexin A2, and annexin A5.ConclusionsThe proteomic alterations described here may suggest that these changes to protein expression correlate with IBV virus' virulence in chicken, hence provides valuable insights into the interactions of IBV with its host and may also assist with investigations of the pathogenesis of IBV and other coronavirus infections.

Variation of vlhA gene in Mycoplasma synoviae clones isolated from chickens

Mycoplasma synoviae synthesizes haemagglutinin VlhA, which cleaves into the N-terminal part, a lipoprotein MSPB, and a C-terminal part MSPA. Previous studies have shown that the 3′-end of the expressed vlhA gene can recombine with vlhA pseudogenes in a process called gene conversion, but there have been no data about diversification of the expressed vlhA gene in M. synoviae populations replicating in chickens. Following intratracheal inoculation with the M. synoviae strain ULB 02/T6, which showed only minor vlhA gene variation prior to inoculation, we investigated temporal changes in MSPB epitopes defined by monoclonal antibodies (mAbs) 3B4 and 50, as well as diversification of the vlhA gene sequence in M. synoviae populations recovered from chicken tracheas. In cultures isolated 8 and 18 days post inoculation (p.i.), most colonies showed variation of MSPB epitopes for mAbs 3B4 and 50. They also changed 3′-end vlhA gene sequences. Further diversity of the vlhA gene occurred in cultures isolated 8 weeks and 5 months p.i. The vlhA gene sequences from isolated cultures shared only 65 to 80% sequence identity with vlhA gene of the inoculated ULB 02/T6 culture. Notably, in most of those cultures their vlhA gene sequences contained stop codons potentially causing premature terminations of translation. Interestingly, in one culture isolated 8 weeks p.i. (clone T6-8W/IT2A) the 3′-vlhA gene sequence was identical in the last 1140 bases to that of the first vlhA pseudogene positioned the most far (upstream) of the expressed vlhA gene. This is the first demonstration of temporal diversity of the vlhA gene in M. synoviae populations isolated from chicken tracheas.

Neuraminidase of Mycoplasma synoviae desialylates heavy chain of the chicken immunoglobulin G and glycoproteins of chicken tracheal mucus

Major poultry pathogens, Mycoplasma gallisepticum and Mycoplasma synoviae share several genes, including nanH that encodes their sialidases (neuraminidases). Previous studies have shown considerable differences in neuraminidase enzymatic activity (NEAC) in M. synoviae strains and NEAC absence in individual cultures of two strains, ULB 925 and ULB 9122. The present study shows that the cultures lacking NEAC did not express NanH neuraminidase detectable by specific antibodies. In cultures of M. synoviae ULB 925 and ULB 9122, which lacked NEAC and detectable NanH, deletions of a single adenine in different nanH regions of each strain created translational frameshifts resulting in TAA (UAA) stop codons and premature termination of translation. ULB 925 and ULB 9122 with such nanH mutations did not desialylate reference fetuin and transferrin or chicken glycoproteins that M. synoviae strains with NEAC efficiently desialylated. They desialylated several chicken serum glycoproteins with SAα(2–6)gal moieties, including the immunoglobulin G heavy chain. Neuraminidase inhibitor 2,3-didehydro-2-deoxy-N-acetylneuraminic acid inhibited such desialylation otherwise caused by M. synoviae WVU 1853 neuraminidase. WVU 1853 also cleaved sialic acid from SAα(2–3)gal moieties from glycoproteins of mucus from chicken tracheas. This is the first demonstration that M. synoviae desialylates glycoproteins of its host.

Induction of inflammatory cytokines and toll-like receptors in chickens infected with avian H9N2 influenza virus

H9N2 influenza virus is endemic in many Asian countries and is regarded as a candidate for the next human pandemic. Knowledge of the induction of inflammatory responses and toll-like receptors (TLRs) in chickens infected with H9N2 is limited. Here, we show that H9N2 induces pro-inflammatory cytokines such as transforming growth factor-beta 3; tumor necrosis factor-alpha; interferon-alpha, -beta, and gamma; and TLR 1, 2, 3, 4, 5, 7, and 15 in trachea, lung, and intestine of infected chickens. In the lung, TLR-15 was dominantly induced. Taken together, it seems that H9N2 infections efficiently induce inflammatory cytokines and TLRs in trachea, lung and intestine of chickens.

Experimental model for learning in vascular surgery and microsurgery: esophagus and trachea of chicken

This paper proposes a model of training surgical skills using vascular anastomosis in an animal model that simulates the size, consistency and resistance arteries and veins, to use it to chicken trachea and esophagus, respectively. We used chicken necks where the esophagus and trachea were dissected and after preparation were followed every step of the procedure of vascular anastomosis. The flow of the anastomosis was confirmed by direct observation and testing of filling (empty-and-refill test) immediately after the anastomosis. All samples proved to be viable by the criteria described above. For the first time presents an interesting experimental model used to train vascular sutures, because it is endowed with all the necessary requirements for the learning of experimental vascular surgery.

Avian Metapneumovirus Subtype B Experimental Infection and Tissue Distribution in Chickens, Sparrows, and Pigeons

Avian metapneumovirus (aMPV) is a respiratory virus that infects a range of avian hosts, including chickens and turkeys. Migratory and local wild birds are implicated in aMPV spread among farms, countries, and seasonal outbreaks of the disease. A subtype B aMPV isolate from commercial chicken flocks suffering from respiratory disease was experimentally inoculated oculonasally into 7-week old chickens, young pigeons, and sparrows. Chickens showed minimal tracheal rales, whereas pigeons and sparrows were asymptomatic. Shedding of aMPV was detected by reverse transcription polymerase chain reaction on homogenates from nasal turbinates. At 5 days postinfection, 5 of 5 chickens, 2 of 5 pigeons, and 1 of 5 sparrows were positive; at 10 or 15 days, none were positive. At 2 and 5 days, aMPV antigens were localized at the ciliated boarder of respiratory epithelium in nasal cavity and trachea of chickens, as well as to the conjunctival epithelium. Pigeons had detectable viral antigens in only the trachea at 2 and 5 days; sparrow tissues did not show any positive staining. At the end of the experiment, at 21 days postinfection, 14 of 15 inoculated chickens seroconverted against aMPV, but none of the inoculated pigeons or sparrows did. The authors believe that pigeons and sparrows have the ability to transmit the virus between chicken farms, although they do not consider pigeons and sparrows as natural hosts for aMPV, given that they failed to seroconvert. In conclusion, pigeons and sparrows are partially susceptible to aMPV infection, probably acting more as mechanical vectors because infection is only temporary and short-lived.

Erratum to: Identification of differentially expressed miRNAs in chicken lung and trachea with avian influenza virus infection by a deep sequencing approach

Erratum to: Identification of differentially expressed miRNAs in chicken lung and trachea with avian influenza virus infection by a deep sequencing approach

Host Intraspatial Selection of Infectious Bronchitis Virus Populations

Arkansas (Ark)-type infectious bronchitis virus (IBV) subpopulations with an S gene sequence distinct from the vaccine predominant consensus were previously found in the upper respiratory tract of chickens within 3 days after inoculation. This finding indicated that a distinct virus subpopulation was rapidly positively selected by the chicken upper respiratory tract. We hypothesized that during host invasion, the replicating IBV population further changes as it confronts the distinct environments of different tissues, leading to selection of the most fit population. We inoculated 15-day-old chickens with 10(4) 50% embryo infective doses of an Ark-type IBV commercial vaccine via the ocular and nasal routes and characterized the sequences of the S1 gene of IBV contained in tear fluid, trachea, and reproductive tract of individual chickens at different times postinoculation. The predominant IBV phenotype contained in the vaccine (before inoculation) became a minor or nondetectable population at all times in all tissues after replication in the majority of the chickens, corroborating our previous findings. Five new predominant populations designated component (C) 1 through C5, showing distinct nonsynonymous changes, i.e., nucleotide changes resulting in different amino acids encoded and thus in a phenotypic change of the predominant virus population, were detected in the tissues or fluids of individual vaccinated chickens. Due to the different biochemical properties of some amino acids that changed in the S1 glycoprotein, we anticipate that phenotypic shift occurred during the invasion process. Significant differences were detected in the incidence of some distinct IBV predominant populations in tissues and fluids; e.g., phenotype C1 showed the highest incidence in the reproductive tract of the chickens, achieving a significant difference versus its incidence in the trachea (P < 0.05). These results indicate for the first time that IBV undergoes intraspatial variation during host invasion, i.e., the dominant genotype/phenotype further changes during host invasion as the microenvironment of distinct tissues exerts selective pressure on the replicating virus population.

Surveillance and characterization of low pathogenic H5 avian influenza viruses isolated from wild migratory birds in Korea

Migratory waterfowls are the natural reservoir of influenza A viruses. However, interspecies transmission had occasionally caused outbreaks in various hosts including humans. To characterize the genetic origins of H5 avian influenza viruses isolated from migratory birds in South Korea, phylogenetic analysis were conducted. A total of 53 H5 viruses were isolated between October 2005 and November 2008. Full genetic characterization indicated that most of these viruses belong to the Eurasian-like avian lineage. However, some segments of the AB/Korea/W235/07 and the AB/Korea/W236/07 isolates were clustered with North American lineage viruses rather than those of the Eurasian lineage, suggesting the occurrence of reassortment between these two avian virus lineages. Phylogenetic analysis further demonstrated that the H5N2 and H5N3 virus isolates were of the low pathogenicity H5 phenotype. The H5 viruses appear to be antigenically similar to each other, but could be distinguished from a recent HPAI H5N1 (EM/Korea/W149/06) virus by hemagglutinin inhibition (HI) assays. Experimental inoculation of representative viruses indicated that certain isolates, particularly AB/Korea/W163/07 (H5N2), could be detected in trachea and lungs of chickens but none could be transmitted by direct contact. Furthermore, all of the viruses could be detected in mice lung without prior adaptation which is indicative of their pathogenic potential in a mammalian host. Overall, our results emphasize the important role that migratory birds play in the perpetuation, transport, and reassortment of avian influenza viruses stressing the need for continued surveillance of influenza virus activity in these avian populations.

Identification of differentially expressed miRNAs in chicken lung and trachea with avian influenza virus infection by a deep sequencing approach.

BackgroundMicroRNAs (miRNAs) play critical roles in a wide spectrum of biological processes and have been shown to be important effectors in the intricate host-pathogen interaction networks. Avian influenza virus (AIV) not only causes significant economic losses in poultry production, but also is of great concern to human health. The objective of this study was to identify miRNAs associated with AIV infections in chickens.ResultsTotal RNAs were isolated from lung and trachea of low pathogenic H5N3 infected and non-infected SPF chickens at 4 days post-infection. A total of 278,398 and 340,726 reads were obtained from lung and trachea, respectively. And 377 miRNAs were detected in lungs and 149 in tracheae from a total of 474 distinct chicken miRNAs available at the miRBase, respectively. Seventy-three and thirty-six miRNAs were differentially expressed between infected and non-infected chickens in lungs and tracheae, respectively. There were more miRNAs highly expressed in non-infected tissues than in infected tissues. Interestingly, some of these differentially expressed miRNAs, including miR-146, have been previously reported to be associated with immune-related signal pathways in mammals.ConclusionTo our knowledge, this is the first study on miRNA gene expression in AIV infected chickens using a deep sequencing approach. During AIV infection, many host miRNAs were differentially regulated, supporting the hypothesis that certain miRNAs might be essential in the host-pathogen interactions. Elucidation of the mechanism of these miRNAs on the regulation of host-AIV interaction will lead to the development of new control strategies to prevent or treat AIV infections in poultry.

The infection of primary avian tracheal epithelial cells with infectious bronchitis virus

Here we introduce a culture system for the isolation, passaging and amplification of avian tracheal epithelial (ATE) cells. The ATE medium, which contains chicken embryo extract and fetal bovine serum, supports the growth of ciliated cells, goblet cells and basal cells from chicken tracheas on fibronectin- or matrigel-coated dishes. Non-epithelial cells make up less than 10% of the total population. We further show that ATE cells support the replication and spread of infectious bronchitis virus (IBV). Interestingly, immunocytostaining revealed that basal cells are resistant to IBV infection. We also demonstrate that glycosaminoglycan had no effect on infection of the cells by IBV. Taken together, these findings suggest that primary ATE cells provide a novel cell culture system for the amplification of IBV and the in vitro characterization of viral cytopathogenesis.

Protection of chickens against infectious bronchitis by a recombinant fowlpox virus co-expressing IBV-S1 and chicken IFNγ

A fowlpox virus expressing the chicken infectious bronchitis virus (IBV) S1 gene of the LX4 strain (rFPV-IBVS1) and a fowlpox virus co-expressing the S1 gene and the chicken type II interferon gene (rFPV-IBVS1-ChIFNγ) were constructed. These viruses were assessed for their immunological efficacy on specific-pathogen-free (SPF) chickens challenged with a virulent IBV. Although the antibody levels in the rFPV-IBVS1-ChIFNγ-vaccinated group were lower than those in the attenuated live IB vaccine H120 group and the rFPV-IBVS1 group, the rFPV-IBVS1-ChIFNγ provided the strongest protection against an IBV LX4 virus challenge (15 out of 16 chickens immunized with rFPV-IBVS1-ChIFNγ were protected), followed by the attenuated live IB vaccine (13/16 protected) and the rFPV-IBVS1 (12/16 protected). Compared to those of the rFPV-IBVS1 and the attenuated live IB vaccine groups, chickens in the rFPV-IBVS1-ChIFNγ group eliminated virus more quickly and decreased the presence of viral antigen more significantly in renal tissue. Examination of affected tissues revealed abnormalities in the liver, spleen, kidney, lung and trachea of chickens vaccinated with the attenuated live IB vaccine and the rFPV-IBVS1 vaccine. In rFPV-IBVS1-ChIFNγ-vaccinated chickens, pathological changes were also observed in those organs, but were milder and lasted shorter. The lesions in the mock control group were the most severe and lasted for at least 20 days. This study demonstrated that chicken type II interferon increased the immunoprotective efficacy of rFPV-IBVS1-ChIFNγ and normal weight gain in vaccinated chickens although it inhibited serum antibody production.