Abstract
We have shown previously that replacement of the spike (S) gene of the apathogenic IBV strain Beau-R with that from the pathogenic strain of the same serotype, M41, resulted in an apathogenic virus, BeauR-M41(S), that conferred protection against challenge with M41 [1]. We have constructed a recombinant IBV, BeauR-4/91(S), with the genetic backbone of Beau-R but expressing the spike protein of the pathogenic IBV strain 4/91(UK), which belongs to a different serogroup as Beaudette or M41. Similar to our previous findings with BeauR-M41(S), clinical signs observations showed that the S gene of the pathogenic 4/91 virus did not confer pathogenicity to the rIBV BeauR-4/91(S). Furthermore, protection studies showed there was homologous protection; BeauR-4/91(S) conferred protection against challenge with wild type 4/91 virus as shown by the absence of clinical signs, IBV RNA assessed by qRT-PCR and the fact that no virus was isolated from tracheas removed from birds primarily infected with BeauR-4/91(S) and challenged with IBV 4/91(UK). A degree of heterologous protection against M41 challenge was observed, albeit at a lower level.Our results confirm and extend our previous findings and conclusions that swapping of the ectodomain of the S protein is a precise and effective way of generating genetically defined candidate IBV vaccines.
Highlights
Avian infectious bronchitis virus (IBV) is a gammacoronavirus, subfamily Coronavirinae, family Coronaviridae, Order Nidovirales [2] and is the aetiological agent of the acute highly contagious poultry disease infectious bronchitis (IB) [3,4,5,6]
We have previously shown, using our IBV reverse genetics system [27,28,29], that replacement of the ectodomain of the IBV Beaudette S glycoprotein with the corresponding region from the pathogenic IBV M41-chick kidney (CK) did not confer virulence to Beau-R but did result in a rIBV, BeauR-M41(S), which had the tissue tropism associated with M41-CK [30]
Chickens that were vaccinated with BeauR-M41(S) were found to be protected against clinical disease following challenge with IBV M41-CK, whereas chickens vaccinated with Beau-R were not protected against challenge with M41-CK [1]. These results indicated that BeauR-M41(S) was able to induce a protective response against homologous challenge with M41-CK, whereas Beau-R was unable to induce a protective response even though both viruses belong to the same, Massachusetts, serogroup
Summary
Avian infectious bronchitis virus (IBV) is a gammacoronavirus, subfamily Coronavirinae, family Coronaviridae, Order Nidovirales [2] and is the aetiological agent of the acute highly contagious poultry disease infectious bronchitis (IB) [3,4,5,6]. IBV is primarily associated with respiratory tract infections, it is responsible for major economic losses to poultry industries worldwide as a result of poor weight gain and decreased egg production [9]. IBV, like all coronaviruses, contains the four structural proteins; spike glycoprotein (S), small membrane protein (E), integral membrane protein (M) and nucleocapsid protein (N), which interacts with the genomic RNA. The S protein is assembled into virion membranes, through non-covalent interactions with the M protein [18], and is responsible for binding to the target cell receptor and fusion of the viral and cellular membranes, fulfilling a major role in the infection of susceptible cells [19]
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