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      Infectious bronchitis virus: Immunopathogenesis of infection in the chicken.

      Avian Pathology

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          Abstract

          The immunopathogenesis of infectious bronchitis virus (IBV) infection in the chicken is reviewed. While infectious bronchitis (IB) is considered primarily a disease of the respiratory system, different IBV strains may show variable tissue tropisms and also affect the oviduct and the kidneys, with serious consequences. Some strains replicate in the intestine but apparently without pathological changes. Pectoral myopathy has been associated with an important recent variant. Several factors can influence the course of infection with IBV, including the age, breed and nutrition of the chicken, the environment and intercurrent infection with other infectious agents. Immunogenic components of the virus include the S (spike) proteins and the N nucleoprotein. The humoral, local and cellular responses of the chicken to IBV are reviewed, together with genetic resistance of the chicken. In long-term persistence of IBV, the caecal tonsil or kidney have been proposed as the sites of persistence. Antigenic variation among IBV strains is related to relatively small differences in amino acid sequences in the S1 spike protein. However, antigenic studies alone do not adequately define immunological relationships between strains and cross-immunisation studies have been used to classify IBV isolates into 'protectotypes'. It has been speculated that changes in the S1 protein may be related to differences in tissue tropisms shown by different strains. Perhaps in the future, new strains of IBV may arise which affect organs or systems not normally associated with IB.

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          Location of antigenic sites defined by neutralizing monoclonal antibodies on the S1 avian infectious bronchitis virus glycopolypeptide.

          Neutralizing monoclonal antibodies directed against five antigenic sites on the spike (S) S1 glycopolypeptide of avian infectious bronchitis virus (IBV) were used to select neutralization-resistant variants of the virus. By comparing the nucleotide sequence of such variants with the sequence of the IBV parent strain, we located five antigenic sites on the amino acid sequence of the S1 glycopolypeptide. The variants had mutations within three regions corresponding to amino acid residues 24 to 61, 132 to 149 and 291 to 398 of the S1 glycopolypeptide. The location of three overlapping antigenic sites on the IBV spike protein was similar to the location of antigenic sites on the spike protein of other coronaviruses.
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            Location of the amino acid differences in the S1 spike glycoprotein subunit of closely related serotypes of infectious bronchitis virus.

            Four UK strains of three different serotypes were found to differ by only 2-3% of their S1 amino acids. The S1 sequences were also very similar to those of three Dutch isolates (D207, D274 and D3896), the greatest difference between two of the seven isolates being 4.4%. The few amino acid differences between the seven isolates were located largely between residues 19-122 and 251-347 of the mature S1 subunit. The seven isolates could be differentiated using 16 monoclonal antibodies in an enzyme-linked immunosorbent assay. Some virus neutralizing (VN) antibody-inducing epitopes were common to all seven isolates even though the strains had been differentiated into three serotypes by polyclonal sera. The results indicate that the most antigenic of the VN antibody-inducing epitopes are formed by very few amino acids and that these occur in the first and third quarters of the S1 subunit. We suggest that serology-based epizootiological studies of IBV should, therefore, be augmented by the inclusion of nucleic acid sequencing and/or monoclonal antibody analysis.
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              Coronavirus IBV: virus retaining spike glycopolypeptide S2 but not S1 is unable to induce virus-neutralizing or haemagglutination-inhibiting antibody, or induce chicken tracheal protection.

              Avian infectious bronchitis coronavirus (IBV) inactivated by beta-propiolactone induced partial protection of the trachea in up to 40% of chickens following one intramuscular inoculation 4 to 6 weeks prior to challenge. Retention of an intact tracheal ciliated epithelium 4 days after challenge was the criterion of protection. There was no correlation between protection and serum titres of virus-neutralizing (VN) and haemagglutination-inhibiting (HI) antibody, which were maximal at about 4 weeks after inoculation. Virus from which the S1 but not the S2 (spike-anchoring) spike glycopolypeptide had been removed by urea did not induce protection or VN or HI antibody. Four intramuscular inoculations of monomeric S1 induced VN and HI antibody in two and four chickens respectively. These results indicate that VN and HI antibodies are induced primarily by S1, that intact spikes are a major requirement for the induction of protective immunity and that this property is probably associated with S1.
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                Journal
                18483939
                10.1080/03079459708419246

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