Abstract:Infectious bronchitis virus (IBV) is a major viral pathogen of commercial poultry, affecting chickens of all ages and causing major economic losses in poultry industry worldwide. Frequent points of mutations and recombination events in the S1 gene region, result in the emergence of new IBVs variants circulating in the form of several serotypes/genotypes that can be partially or poorly neutralized by current vaccines. IBV is well studied worldwide, nevertheless in African countries epidemiological and scientifi… Show more
“…QX like IBV strains) and Mass type IBV isolates recovered from various geographical areas [18,42,43,45,46]. Nephropathogenic QX-type strains are distantly related to the M41 strain and their genetic similarity is 78.6% [60]. Based on the partial S1 sequence analysis of three nephropathogenic IBV isolates, which belong to the Mass genotype revealed that they are more than 99.1 and 97.8% identical to the classical M41 strain in nucleotide and deduced amino acid sequences, respectively [61].…”
BackgroundInfectious bronchitis virus (IBV) is one of the leading causes of mortality and morbidity in chickens. There are numerous serotypes and variants, which do not confer cross protection resulting in failure of currently used IBV vaccines. Although variant IBV isolates with major genetic differences have been subjected to comparative studies, it is unknown whether minor genetic differences in IBV variants within a serotype are different in terms of pathogenesis and eliciting host responses. Two Massachusetts (Mass) variant IBV isolates recovered from commercial layer flocks in the Western Canadian provinces of Alberta (AB) and Saskatchewan (SK) were compared genetically and evaluated for their pathogenicity, tissue distribution and ability to recruit and replicate in macrophages.ResultsAlthough whole genome sequencing of these two Mass IBV isolates showed low similarity with the M41 vaccinal strain, they had an identical nucleotide sequence at open reading frames (ORFs) 3a, 3b, envelop (E), matrix (M), 5a and 5b. The rest of the ORFs of these 2 IBV isolates showed 99.9% nucleotide similarity. However, upon experimental infection, we found that the IBV isolate originating from AB was different to the one that originated in SK due to higher tracheal lesion scores and lower lung viral replication and lower genome loads in cecal tonsils. Nevertheless, both IBV isolates elicited host responses characterized by significant macrophage recruitment to the respiratory tract and there was evidence that both IBV isolates replicated within tracheal and lung macrophages.ConclusionsOverall, this study shows that Mass variant IBV isolates, although possessing minor genetic variations, can lead to significant differences in pathogenicity in young chickens. Further studies are required to investigate the pathogenicity of these two Mass variant IBV isolates in laying hens.Electronic supplementary materialThe online version of this article (10.1186/s12917-018-1720-9) contains supplementary material, which is available to authorized users.
“…QX like IBV strains) and Mass type IBV isolates recovered from various geographical areas [18,42,43,45,46]. Nephropathogenic QX-type strains are distantly related to the M41 strain and their genetic similarity is 78.6% [60]. Based on the partial S1 sequence analysis of three nephropathogenic IBV isolates, which belong to the Mass genotype revealed that they are more than 99.1 and 97.8% identical to the classical M41 strain in nucleotide and deduced amino acid sequences, respectively [61].…”
BackgroundInfectious bronchitis virus (IBV) is one of the leading causes of mortality and morbidity in chickens. There are numerous serotypes and variants, which do not confer cross protection resulting in failure of currently used IBV vaccines. Although variant IBV isolates with major genetic differences have been subjected to comparative studies, it is unknown whether minor genetic differences in IBV variants within a serotype are different in terms of pathogenesis and eliciting host responses. Two Massachusetts (Mass) variant IBV isolates recovered from commercial layer flocks in the Western Canadian provinces of Alberta (AB) and Saskatchewan (SK) were compared genetically and evaluated for their pathogenicity, tissue distribution and ability to recruit and replicate in macrophages.ResultsAlthough whole genome sequencing of these two Mass IBV isolates showed low similarity with the M41 vaccinal strain, they had an identical nucleotide sequence at open reading frames (ORFs) 3a, 3b, envelop (E), matrix (M), 5a and 5b. The rest of the ORFs of these 2 IBV isolates showed 99.9% nucleotide similarity. However, upon experimental infection, we found that the IBV isolate originating from AB was different to the one that originated in SK due to higher tracheal lesion scores and lower lung viral replication and lower genome loads in cecal tonsils. Nevertheless, both IBV isolates elicited host responses characterized by significant macrophage recruitment to the respiratory tract and there was evidence that both IBV isolates replicated within tracheal and lung macrophages.ConclusionsOverall, this study shows that Mass variant IBV isolates, although possessing minor genetic variations, can lead to significant differences in pathogenicity in young chickens. Further studies are required to investigate the pathogenicity of these two Mass variant IBV isolates in laying hens.Electronic supplementary materialThe online version of this article (10.1186/s12917-018-1720-9) contains supplementary material, which is available to authorized users.
“…Effective vaccination against IBV is proving to be an increasing challenge due to the emergence of novel strains, such as QX, first isolated in China, in 1995 [ 29 ], and subsequently spread worldwide [ 30 , 31 , 32 ]. Whilst some strains of IBV have spread worldwide, others have emerged but remained limited to distinct geographical areas [ 33 , 34 ]. Commercial live IBV vaccines are generated through multiple passages of a pathogenic field isolate through embryonated hen’s eggs with the aim of generating a virus that is attenuated but still immunogenic [ 35 , 36 ].…”
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.
“…It is an enveloped positive-stranded RNA virus with a genome of about 27.6 kb in length encompassing 5 0 and 3 0 untranslated regions with a poly(A) tail. A major part of the genome is composed of two overlapping open reading frames (ORFs), 1a and 1b, which are translated into large polyproteins, 1a and 1ab, respectively, and contribute to the formation of the replication and transcription complex (Cavanagh., 1997;Khataby et al, 2016b). The remaining part of the genome encodes for four structural proteins that are called the phosphorylated nucleocapsid protein (N), the membrane glycoprotein (M), the envelope protein (E), and the spike glycoprotein (S).…”
Section: Introductionmentioning
confidence: 99%
“…The high variation in the nucleotide sequences of spike gene can change the protection ability of a vaccine or immunity (Cavanagh and Naqi, 2003). Some reports have demonstrated that this genetic diversity, due to changed genomic virus by frequent point mutations and recombination events in the S1 gene, has given the emergence of new IBV variants that can be partially or poorly neutralized by existing vaccine serotypes (Khataby et al, 2016b). Wherefore, the phylogenetic analysis of the S1 gene is the most useful strategy to differentiate IBV genotypes and serotypes, because it correlates closely with the serotype and permits the selection of the appropriate vaccine serotypes for IB control in each of the geographic regions (Jackwood, 2012).…”
Section: Introductionmentioning
confidence: 99%
“…The evolutionary characterization of IBV is essentially based on the analysis of the variable S1 gene or the expressed S1 protein. Moreover, three hypervariable regions (HVR1, HVR2, and HVR3) located at the positions 114À201, 297À423, and 822À1161 nt corresponding respectively, to amino acid residues 38À67, 91À141, and 274À387 have been located within the S1 subunit (Bourogâa et al, 2009;Khataby et al, 2016b).…”
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