Coronavirus IBV: Removal of Spike Glycopolypeptide S1 by Urea Abolishes Infectivity and Haemagglutination but Not Attachment to Cells

Cavanagh, David; Davis, Philip J.

doi:10.1099/0022-1317-67-7-1443

Cited by 162 publications

(135 citation statements)

References 19 publications

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“…The IBV spike (S) protein is responsible for viral attachment to the host cell and is a relevant target for specific humoral and cellular host immune responses (Cavanagh, 1981(Cavanagh, , 1983(Cavanagh, , 1984Mockett et al, 1984;Cavanagh & Davis, 1986;Collisson et al, 2000). The bulb end of the S protein (S1) exhibits extensive variation among IBV populations (Kusters et al, 1987(Kusters et al, , 1989, providing a successful adaptation favouring immunological escape.…”

Section: Introductionmentioning

confidence: 99%

Effects of chicken anaemia virus and infectious bursal disease virus-induced immunodeficiency on infectious bronchitis virus replication and genotypic drift

2012

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We followed changes in a portion of the S1 gene sequence of the dominant populations of an infectious bronchitis virus (IBV) Arkansas (Ark) vaccine strain during serial passage in chickens infected with the immunosuppressive chicken anaemia virus (CAV) and/or infectious bursal disease virus (IBDV) as well as in immunocompetent chickens. The IBV-Ark vaccine was applied ocularly and tears were collected from infected chickens for subsequent ocular inoculation in later passages. The experiment was performed twice. In both experiments the dominant S1 genotype of the vaccine strain was rapidly and negatively selected in all chicken groups (CAV, IBDV, CAV'IBDV and immunocompetent). Based on the S1 genotype, the same IBV subpopulations previously reported in immunocompetent chickens and named component (C) 1 to C5 emerged both in immunocompetent and immunodeficient chickens. During the first passage different subpopulations emerged, followed by the establishment of one or two predominant populations after further passages. Only when the subpopulation designated C2 became established in either CAV-infected or IBDVinfected chickens was IBV maintained for more than four passages. These results indicate that selection does not cease in immunodeficient chickens and that phenotype C2 may show a distinct adaptation to this environment. Subpopulations C1 or C4 initially became established in immunocompetent birds but became extinct after only a few succeeding passages. A similar result was observed in chickens co-infected with CAV 'IBDV. These results suggest that the generation of genetic diversity in IBV is constrained. This finding constitutes further evidence for phenotypic drift occurring mainly as a result of selection.

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Section: Introductionmentioning

confidence: 99%

Effects of chicken anaemia virus and infectious bursal disease virus-induced immunodeficiency on infectious bronchitis virus replication and genotypic drift

2012

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“…Mutations occur frequently in hypervariable regions of the S1 subunit of the envelope spike (S) glycoprotein gene. The S1 protein is responsible for infection of the host cell (Cavanagh & Davis, 1986;Koch et al ., 1990;Ignjatovic & Galli, 1994), inducing virusneutralizing antibody (Cavanagh et al ., 1988) and immunity (Cavanagh et al ., 1997). New variant strains may differ as much as 55% in their S1 amino acid sequence compared with vaccine strains (Kusters et al ., 1989;Gelb et al ., 1997).…”

Section: Introductionmentioning

confidence: 99%

S1 gene characteristics and efficacy of vaccination against infectious bronchitis virus field isolates from the United States and Israel (1996 to 2000)

Weisman²,

et al. 2005

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The S1 genes of isolates of avian coronavirus infectious bronchitis virus (IBV) from commercial chickens in the US and Israel (20 isolates from each country) were studied using reverse transcription-polymerase chain reaction restriction fragment length polymorphism and sequencing. Partial sequences spanning the amino terminus region of S1 from amino acid residues 48 to 219, based on the Beaudette strain, were used for analysis. Phylogenetic clustering and high-sequence identity values were used to identify isolates that appeared to be derived from live IBV vaccines used in the two countries. Novel variant strains, unrelated by S1 sequencing and restriction fragment length polymorphism analyses to reference and vaccine strains, were also identified. Based on S1 sequence identity to available vaccines, the potential to use vaccination to control IBV infections was evaluated. Vaccination with commercial live strains Massachusetts (Mass), Arkansas (Ark) or DE/072/92, generally produced immunity against vaccine-related field isolates displaying high S1 sequence similarities (]/90%) to the respective vaccine strains. Immunization with a bivalent vaccine containing the Mass and Ark strains provided good cross-protection, averaging 81% against challenge with five variant isolates from the US having amino acid identity values ranging from 62 to 69% to Mass and from 68 to 83% to Ark, respectively. In contrast, the H120 vaccine strain induced low levels of protection, ranging from 25 to 58% against variant field isolates from Israel with amino acid identity values from 65 to 67%.

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“…Except for the nucleocapsid protein (N), all other structural proteins so far identified are associated with the lipid membrane. The integral membrane protein (M), which is largely embedded in the lipid bilayer targets the site of virus morphogenesis (Tooze et al, 1984) and may be implicated in viral pathogenesis (Fleming et al, 1989), whereas the bulbous peplomer (S) protein is responsible for virus binding (Cavanagh & Davis, 1986;Koch et al, 1990) as well as virulence and tissue tropism (Wege et al, 1988). An additional surface protein (HE), responsible for haemagglutination, has been found in bovine coronavirus (BCV; King et al, 1985;Hogue et al, 1989;Parker et al, 1989), human respiratory coronavirus strain OC43 (HCV-OC43; Hogue & Brian, 1985), haemagglutinating encephalitis virus of swine (Callebaut & Pensaert, 1980), diarrhoea virus of infant mice (Sugiyama et al, 1986) and turkey coronavirus (TCV; Dea et al, 1986).…”

Section: Introductionmentioning

confidence: 99%

Sequence analysis of the turkey enteric coronavirus nucleocapsid and membrane protein genes: a close genomic relationship with bovine coronavirus

Verbeek¹,

Tijssen²

1991

Journal of General Virology

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The 3' end of the turkey coronavirus (TCV) genome and the gene encoding the nucleocapsid protein (N) were cloned and sequenced. The gene encoding the membrane protein (M) was obtained by cloning a polymerase chain reaction (PCR)-amplified fragment obtained using bovine coronavirus (BCV)-specific primers. Furthermore, five TCV DNA fragments, obtained by PCR on RNA from clinical specimens and corresponding to either the N terminus of the M protein or the complete M protein were also cloned and sequenced. The sequence revealed a 3' non-coding region of 291 bases, an open reading frame (ORF) encoding the N protein with a predicted size of 448 amino acids, or an Mr of 49K, and an ORF encoding the M protein with a predicted size of 230 amino acids and an Mr of 26K. A third ORF, encoding a hypothetical protein of 207 amino acids with an Mr of 23K was found within the N gene sequence. The amino acid sequences of both the N and M proteins were more than 99% similar to those published for BCV. Extensive similarity was also observed between the amino acid sequences of the TCV N protein and those of murine hepatitis virus (MHV) (70%) and human respiratory coronavirus strain OC43 (HCV-OC43) (98%) and between the amino acid sequences of the predicted M proteins of TCV and MHV (86 %). Such striking identity suggests that BCV, TCV and HCV-OC43 must have diverged from each other only recently. A potential N-glycosylation site was found at the N terminus of the TCV M protein and is situated at the same location in BCV, MHV and transmissible gastroenteritis virus.

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Coronavirus IBV: Removal of Spike Glycopolypeptide S1 by Urea Abolishes Infectivity and Haemagglutination but Not Attachment to Cells

Cited by 162 publications

References 19 publications

Effects of chicken anaemia virus and infectious bursal disease virus-induced immunodeficiency on infectious bronchitis virus replication and genotypic drift

Effects of chicken anaemia virus and infectious bursal disease virus-induced immunodeficiency on infectious bronchitis virus replication and genotypic drift

S1 gene characteristics and efficacy of vaccination against infectious bronchitis virus field isolates from the United States and Israel (1996 to 2000)

Sequence analysis of the turkey enteric coronavirus nucleocapsid and membrane protein genes: a close genomic relationship with bovine coronavirus

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