Infectious bronchitis virus strain:M41-CK
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PROVIDER: PRJNA722374 | ENA |
REPOSITORIES: ENA
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Project description:Infection of chicken coronavirus infectious bronchitis virus (IBV) is initiated by binding of the viral heavily N-glycosylated attachment protein spike to the alpha-2,3-linked sialic acid receptor Neu5Ac. Previously, we have shown that N-glycosylation of recombinantly expressed receptor binding domain (RBD) of the spike of IBV-M41 is of critical importance for binding to chicken trachea tissue. Here we investigated the role of N-glycosylation of the RBD on receptor specificity and virus replication in the context of the virus particle. Using our reverse genetics system we were able to generate recombinant IBVs for nine-out-of-ten individual N-glycosylation mutants. In vitro growth kinetics of these viruses were comparable to the virus containing the wild-type M41-S1. Furthermore, Neu5Ac binding by the recombinant viruses containing single N-glycosylation site knock-out mutations matched the Neu5Ac binding observed with the recombinant RBDs. Five N-glycosylation mutants lost the ability to bind Neu5Ac and gained binding to a different, yet unknown, sialylated glycan receptor on host cells. These results demonstrate that N-glycosylation of IBV is a determinant for receptor specificity.
| S-EPMC7414442 | biostudies-literature
Project description:Infectious bronchitis virus (IBV) is a pathogenic coronavirus with high morbidity and mortality in chicken breeding. Macrophages with normal biofunctions are essential for host immune responses. In this study, the HD11 chicken macrophage cell line and chicken peripheral blood mononuclear cell-derived macrophages (PBMCs-Mφ) were infected with IBV at multiplicity of infection (MOI) of 10. The dynamic changes of their biofunctions, including cell viability, pathogen elimination function, phagocytic ability, and gene expressions of related proteins/mediators in innate and acquired immunity, inflammation, autophagy and apoptosis were analyzed. Results showed that IBV infection decreased chicken macrophage viability and phagocytic ability, and increased pathogen elimination function. Moreover, IBV augmented the gene expressions of most related proteins in macrophages involved in multiple host bioprocesses, and the dynamic changes of gene expressions had a close relationship with virus replication. Among them, MHCII, Fc receptor, TLR3, IFN-α, CCL4, MIF, IL-1β, IL-6, and iNOS showed significantly higher expressions in IBV-infected cells. However, TLR7, MyD88, MDA5, IFN-γ, MHCII, Fc receptor, MARCO, CD36, MIF, XCL1, CXCL12, TNF-α, iNOS, and IL-10 showed early decreased expressions. Overall, chicken macrophages play an important role in host innate and acquired immune responses to resist IBV infection, despite early damage or suppression. Moreover, the IBV-induced autophagy and apoptosis might participate in the virus-host cell interaction which is attributed to the biological process.
| S-EPMC7841764 | biostudies-literature
Project description:Infectious bronchitis virus (IBV) is a very dynamic and evolving virus, causing major economic losses to the global poultry industry. In early 2011, respiratory disease outbreaks were investigated in Iraq, Jordan, and Saudi Arabia. Five IBV isolates (JOA2, JOA4, Saudi-1, Saudi-2, and Iraqi IBV) were detected by diagnostic-nested nucleocapsid RT-PCR. Strain identification was characterised by sequencing and phylogenetic analysis of the amplified hypervariable region of the spike 1 (S1) gene. These five IBV isolates were found to be of the IBV strain CK/CH/LDL/97I. Nucleotide identity between these five IBV isolates ranged from 96.9% to 99.7%, and between these isolates and the CK/CH/LDL/97I strain in the range of 96.6-99.1%. The sequenced fragment of the S1 gene of the CK/CH/LDL/97I strain had less than 80% nucleotide identity to the IBV vaccine strains commonly used in the Middle East (M41 and H120). The presence of these CK/CH/LDL/97I-like strains may account for vaccination failure against IBV, since all IBV isolates were from vaccinated chickens. In this paper, we documented for the first time the presence of IBV strain CK/CH/LDL/97I in the Middle East. This strain is known to have originated in China and Taiwan.
| S-EPMC3658599 | biostudies-literature
Project description:Recombination among infectious bronchitis viruses (IBVs), coupled with point mutations, insertions, and deletions that occur in the genome, is thought to contribute to the emergence of new IBV variants. In this study an IBV, ck/CH/LJL/111054, was isolated from a H120-vaccinated chicken, which presented with a suspected IBV infection. Phylogenetic analysis of the S1 subunit sequence confirmed that strain ck/CH/LJL/111054 is of the Connecticut-type; however, further extensive full-length genomic analysis identified the occurrence of recombination events. Therefore, strain ck/CH/LJL/111054 may have originated from recombination events between Conn- and Mass-like strains at three recombination breakpoints: two located within the nsp3 gene sequence and one in the nsp12 gene sequence. Further, the uptake of the 5' untranslated regions, nsp2, parts of nsp3, nsp4-11, and parts of nsp 12 from Mass-like virus by ck/CH/LJL/111054 might have resulted in changes in viral replication efficiency rather than antigenic changes, via cross-neutralization analysis with the H120 strain. Recombination events coupled with the accumulation of mutations in the ck/CH/LJL/111054 genome may account for its increased virulence in specific-pathogen free chickens.
| S-EPMC7106169 | biostudies-literature
Project description:BackgroundWe previously attenuated the infectious bronchitis virus (IBV) strain CK/CH/LDL/97I and found that it can convey protection against the homologous pathogenic virus.ObjectiveTo compare the full-length genome sequences of the Chinese IBV strain CK/CH/LDL/97I and its embryo-passaged, attenuated level to identify sequence substitutions responsible for the attenuation and define markers of attenuation.MethodsThe full-length genomes of CK/CH/LDL/97I P5 and P115 were amplified and sequenced. The sequences were assembled and compared using the MEGALIGN program (DNAStar) and a phylogenetic tree was constructed using MEGA4 software.ResultsThe CK/CH/LDL/97I virus population contained subpopulations with a mixture of genetic mutants. Changes were observed in nsp4, nsp9, nsp11/12, nsp14, nsp15, nsp16, and ORF3a, but these did not result in amino acid substitutions or did not show functional variations. Amino acid substitutions occurred in the remaining genes between P5 and P115; most were found in the S region, and some of the nucleotide mutations resulted in amino acid substitutions. Among the 9 nsps in the ORF1 region, nsp3 contained the most nucleotide substitutions.ConclusionsSequence variations in different genes, especially the S gene and nsp3, in the genomes of CK/CH/LDL/97I viruses might contribute to differences in viral replication, pathogenicity, antigenicity, immunogenicity, and tissue tropism.
| S-EPMC7179551 | biostudies-literature
Project description:Infectious bronchitis virus (IBV), is a coronavirus which infects chickens (Gallus gallus), and is one of the foremost causes of economic loss within the poultry industry, affecting the performance of both meat-type and egg-laying birds. The virus replicates not only in the epithelium of upper and lower respiratory tract tissues, but also in many tissues along the alimentary tract and elsewhere e.g. kidney, oviduct and testes. It can be detected in both respiratory and faecal material. There is increasing evidence that IBV can infect species of bird other than the chicken. Interestingly breeds of chicken vary with respect to the severity of infection with IBV, which may be related to the immune response (Cavanagh, 2006). Here we examine differential expression of genes in the trachea of susceptible and resistant birds, in order to identify genes which may be involved in resistance to IBV.
2015-07-31 | E-TABM-1128 | biostudies-arrayexpress
Project description:Avian infectious bronchitis (IB) is caused by avian infectious bronchitis virus (IBV) belonging to Coronaviridae family. The disease is prevalent in all countries with almost 100% incidence rate. Chicken and commercially reared pheasant are the natural host for IBV. Virus causes respiratory diseases, poor weight gain, feed efficiency in broiler, damage to oviduct, and abnormal egg production in mature hens resulting in economic losses. IBV also replicates in tracheal and renal epithelial cells leading to prominent tracheal and kidney lesions. Virus undergoes spontaneous mutation leading to continual emergence of new variants. The effectiveness of immunization program is diminished because of poor cross-protection among the serotypes. Identification of circulating serotypes is important in controlling IBV infection. Toll-like receptor 3 (TLR3) and TLR21 are involved in early recognition of virus resulting in induction of inflammatory cytokines. Both humoral and cellular immune responses are important in the control of infection. Humoral immunity plays an important role in recovery and clearance of viral infection. IBV-specific cytotoxic T lymphocytes induce lysis of IBV-infected cells. Effective diagnostic tools are required at field level to identify different IBV variants. Embryonated chicken eggs are effective model for virus isolation. Identification by other specific methods like virus neutralization (VN), hemagglutination inhibition (HI), enzyme linked immunosorbent assay (ELISA), immunohistochemistry, or nucleic acid analysis or by electron microscopy is also indispensable. VN test in tracheal organ culture is the best method for antigenic typing for surveillance purposes. Continuous epidemiological surveillance, strict biosecurity measures, and vaccine effective against various serotypes are necessary for controlling IB in chickens.
| S-EPMC7120852 | biostudies-literature
Project description:Avian infectious bronchitis virus (IBV) causes tremendous economic losses to the poultry industry worldwide. Different serotypes of this virus show little cross-protection. The present study investigated the genotypic relationship between CK/CH/LDL/97I-type strains and reference IBVs based on S1 gene comparisons and the protection provided by vaccination with commercial vaccines and attenuated homologous and heterologous strains. Phylogenetic analysis and the comparison of S1 showed that CK/CH/LDL/97I-type virus might be a new serotype compared to vaccine strains and other types of IBV isolates in China. Protection efficacy was evaluated by morbidity, mortality, and virus re-isolation from the challenged chicks. Complete protection by IBV vaccination was provided by the homologous strain but sufficient respiratory protection was not provided by the commercial vaccines. Heterologous strains against CK/CH/LDL/97I challenge and the development of a vaccine against CK/CH/LDL/97I-type IBV will be necessary to control infectious bronchitis disease in poultry. Further development of the attenuated CK/CH/LDL/97I strain may provide a valuable contribution towards this goal.
| S-EPMC7110898 | biostudies-literature
Project description:Background: Avian infectious bronchitis (IB) is an acute and highly contagious disease of the upper-respiratory tract caused by infectious bronchitis virus (IBV). Understanding the molecular mechanisms involved in the interaction between innate and adaptive immune responses to IBV infection is a crucial element for further improvements in strategies to control IB. To this end, two chicken lines, selected for high and low serum concentration of mannose-binding lectin (MBL), a soluble pattern recognition receptor, were studied. In total, 32 birds from each line (designated L10H for high and L10L for low MBL serum concentration, respectively) were used. Sixteen birds from each line were infected with IBV at 3 weeks of age and sixteen birds were left uninfected. Eight uninfected and eight infected birds from each line were euthanized at 1 and 3 weeks post infection. RNA sequencing was performed on spleen samples from all 64 birds used in the experiment. Differential gene expression analysis was performed for four comparisons: L10L line versus L10H line for uninfected birds at weeks 1 and 3, respectively, and L10L line versus L10H line for infected birds at weeks 1 and 3, respectively. Functional analysis based on the differentially expressed genes was performed using Gene Ontology (GO) Immune System Process terms specific for Gallus gallus. Results: Comparing uninfected L10H and L10L birds, we identified 1698 and 1424 differentially expressed (DE) genes at weeks 1 and 3, respectively. For the IBV-infected birds, 1934 and 866 DE genes were identified between the two lines at weeks 1 and 3, respectively. In both cases DE genes had FDR-adjusted p-value <0.05. The two most enriched GO terms emerging from the comparison of uninfected birds between the two lines were “Lymphocyte activation involved in immune response” (GO:0002285) and “Somatic recombination of immunoglobulin genes involved in immune response” (GO:0002204) at weeks 1 and 3, respectively. When comparing IBV-infected birds between the two lines, the most enriched GO terms were “Alpha-beta T cell activation” (GO:0046631) and “Positive regulation of leukocyte activation” (GO:0002696) at weeks 1 and 3, respectively. Conclusion: Healthy birds from the two lines showed significant differences in expression profiles for subsets of both adaptive and innate immunity-related genes, whereas comparison of the IBV-infected birds from the two lines showed differences in expression of immunity-related genes involved in T cell activation and proliferation. The observed transcriptome differences between the two lines indicate that selection for MBL had a much wider effect than solely on serum MBL concentration, and in addition influenced the innate and adaptive immune responses. Future research will focus on identifying signatures of selection in order to further understand molecular pathways be responsible for differences between the two lines as well as for efficient IBV immune protection.
2016-01-25 | GSE73423 | GEO
Project description:Gammacoronavirus infectious bronchitis virus (IBV) causes an economically important respiratory disease of poultry. Protective immunity is associated with the major structural protein, spike (S) glycoprotein, which induces neutralising antibodies and defines the serotype. Cross-protective immunity between serotypes is limited and can be difficult to predict. In this study, the ability of two recombinant IBV vaccine candidates, BeauR-M41(S) and BeauR-4/91(S), to induce cross-protection against a third serotype, QX, was assessed. Both rIBVs are genetically based on the Beaudette genome with only the S gene derived from either M41 or 4/91, two unrelated serotypes. The use of these rIBVs allowed for the assessment of the potential of M41 and 4/91 S glycoproteins to induce cross-protective immunity against a heterologous QX challenge. The impact of the order of vaccination was also assessed. Homologous primary and secondary vaccination with BeauR-M41(S) or BeauR-4/91(S) resulted in a significant reduction of infectious QX load in the trachea at four days post-challenge, whereas heterologous primary and secondary vaccination with BeauR-M41(S) and BeauR-4/91(S) reduced viral RNA load in the conjunctiva-associated lymphoid tissue (CALT). Both homologous and heterologous vaccination regimes reduced clinical signs and birds recovered more rapidly as compared with an unvaccinated/challenge control group. Despite both rIBV BeauR-M41(S) and BeauR-4/91(S) displaying limited replication in vivo, serum titres in these vaccinated groups were higher as compared with the unvaccinated/challenge control group. This suggests that vaccination with rIBV primed the birds for a boosted humoral response to heterologous QX challenge. Collectively, vaccination with the rIBV elicited limited protection against challenge, with failure to protect against tracheal ciliostasis, clinical manifestations, and viral replication. The use of a less attenuated recombinant vector that replicates throughout the respiratory tract could be required to elicit a stronger and prolonged protective immune response.
| S-EPMC7350270 | biostudies-literature