Chicken interferons, their receptors and interferon-stimulated genes

Goossens, Kate E.; Ward, Alister C.; Lowenthal, John W.; Bean, Andrew G.D.

doi:10.1016/j.dci.2013.05.020

Cited by 52 publications

(66 citation statements)

References 117 publications

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“…It has been recently revealed in evolutionary and comparative immunology that introns were lost from primitive intron-containing type I IFN genes in fish and amphibians, and intronless type I IFN genes were evolved in amniotes (Chen et al, 2015;Goossens et al, 2013;Grayfer et al, 2014;Sang et al, 2014;Xu et al, 2013;Zou and Secombes, 2011;Zou et al, 2007); but it remains unclear how this process might have occurred (Zou et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

“…In mammals, type I IFNs have evolved into at least seven major homologous subgroups, including multigene a subtypes (13 genes in human), and single b, ε, k, t, d, and u subtypes, respectively (Sang et al, 2014;Xu et al, 2013). Interestingly, type I IFNs in mammals, birds and reptiles are encoded by intronless genes, which express single exon transcripts (Goossens et al, 2013;Sang et al, 2014;Xu et al, 2013). In contrast, type I IFN genes in fish and amphibians possess distinct genomic organisation, consisting of five exons and four introns (Chen et al, 2015;Grayfer et al, 2014;Zou and Secombes, 2011;Zou et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Intronless and intron-containing type I IFN genes coexist in amphibian Xenopus tropicalis : Insights into the origin and evolution of type I IFNs in vertebrates

Gan

Chen

Huang

et al. 2017

Developmental & Comparative Immunology

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Intronless and intron-containing type I IFN genes coexist in amphibian Xenopus tropicalis : Insights into the origin and evolution of type I IFNs in vertebrates

Gan

Chen

Huang

et al. 2017

Developmental & Comparative Immunology

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“…A recent study of IFNs in the African clawed frog indicated that type I and III IFNs were already diverged in amphibians, showing five genes of frog IFN-λ and five intron-containing IFN progenitors of type I IFNs located separately in different genomic scaffolds [9]. Genes of avian type I IFNs clearly are intronless, as characterized in about 10 chicken IFN-α and one IFN-β (originally designated as chicken IFN-1 and IFN-2, respectively) [12]. The intronless type I IFNs in amniotes appear to have arisen from a retroposition event that assumedly replaced the original type I IFN locus with intron-spliced RNA, thus favoring subsequent gene duplication and family expansion adaptable to rapidly evolving viruses and multifunctional divergence [9]–[12].…”

Section: Introductionmentioning

confidence: 99%

Molecular Evolution of the Porcine Type I Interferon Family: Subtype-Specific Expression and Antiviral Activity

2014

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Type I interferons (IFNs), key antiviral cytokines, evolve to adapt with ever-changing viral threats during vertebrate speciation. Due to novel pathogenic pressure associated with Suidae speciation and domestication, porcine IFNs evolutionarily engender both molecular and functional diversification, which have not been well addressed in pigs, an important livestock species and animal model for biomedical sciences. Annotation of current swine genome assembly Sscrofa10.2 reveals 57 functional genes and 16 pseudogenes of type I IFNs. Subfamilies of multiple IFNA, IFNW and porcine-specific IFND genes are separated into four clusters with ∼60 kb intervals within the IFNB/IFNE bordered region in SSC1, and each cluster contains mingled subtypes of IFNA, IFNW and IFND. Further curation of the 57 functional IFN genes indicates that they include 18 potential artifactual duplicates. We performed phylogenetic construction as well as analyses of gene duplication/conversion and natural selection and showed that porcine type I IFN genes have been undergoing active diversification through both gene duplication and conversion. Extensive analyses of the non-coding sequences proximal to all IFN coding regions identified several genomic repetitive elements significantly associated with different IFN subtypes. Family-wide studies further revealed their molecular diversity with respect to differential expression and restrictive activity on the resurgence of a porcine endogenous retrovirus. Based on predicted 3-D structures of representative animal IFNs and inferred activity, we categorized the general functional propensity underlying the structure-activity relationship. Evidence indicates gene expansion of porcine type I IFNs. Genomic repetitive elements that associated with IFN subtypes may serve as molecular signatures of respective IFN subtypes and genomic mechanisms to mediate IFN gene evolution and expression. In summary, the porcine type I IFN profile has been phylogenetically defined family-wide and linked to diverse expression and antiviral activity, which is important information for further biological studies across the porcine type I IFN family.

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“…182 The role of the Mx protein is more controversial in the chicken with some studies indicating an important role for Mx in the antiviral response to influenza and others showing that Mx has limited antiviral activity. 180,183,184 However, whilst the definitive role that Mx plays in the defense against ND is not clear, it has been evaluated in this study to further compare the type I IFN pathways induced against NDV isolates of differing pathogenicity. 185 However, the role of cytokines in pathological damage to the host has not yet been elucidated.…”

Section: Discussionmentioning

confidence: 99%

“…179 Binding of TLRs induces the activation of genes encoding cytokine production including the type I interferon family comprising interferon- (IFN-) and interferon-β (IFN-β). 177,180 IFN- and IFN-β, once released, bind to class II cytokine receptors, IFNAR1 and IFNAR2 respectively (Figure 6.1). This activates a signaling cascade via the Janus kinase (Jak) and signal transducer and activation of transcription (STAT) pathway, which results in the activation of IFN-stimulated genes (ISG) which have a wide range of effects, including further cytokine production, cell degranulation and adenosine monophosphate production.…”

Section: Discussionmentioning

confidence: 99%

The molecular basis of the pathogenicity of Newcastle disease virus in chickens

Bergfeld¹

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Newcastle disease (ND) is a highly pathogenic disease of poultry and is caused by virulent strains of Newcastle disease virus (NDV). From 1998From -2002 there were outbreaks of ND in Australia which resulted in significant disruptions to the poultry industry. In some of these outbreaks however, the clinical signs observed in the infected birds did not appear to correlate with the World Organisation for Animal Health's definition of a virulent virus, which is based on the molecular sequence at the fusion protein cleavage site. In one particular outbreak at Meredith, Victoria, in 2002, a virulent virus was isolated, despite only a minimal increase in mortalities on the property. Therefore, this thesis has attempted to determine whether, in addition to the fusion protein cleavage site, there are other molecular determinants of pathogenicity for NDV. NDV. Sequence analysis showed a number of amino acid differences throughout the genomes of the four viruses studied, however none of these differences were in key areas such as glycosylation sites. The Meredith/02 virus was also shown to replicate well in embryonated eggs, throughout the chorioallantoic membrane and internal organs of the embryo, including the lung, liver and kidneys. This is consistent with other virulent NDVs.ii The V protein of the Meredith/02 virus was investigated for its role in potential attenuation of the virus via modulation of the host innate immune response. However there was no difference found in the ability of the Meredith/02 V protein to antagonise type I interferon in-vitro when compared with the Herts 33/56 virus.In an attempt to analyse the viral replication complex, to identify a specific protein that may be involved with the minimal pathogenicity of the Meredith/02 virus, the transcription gradient of the virus was characterized. It was found that the Meredith/02 virus has an increased transcription gradient when compared with the Herts 33/56 virus. The gradient of the Meredith/02 virus was particularly steep at the N-P junction, with particularly low levels of the P gene transcribed at 24 hours. However, gene start and end sequences at this location did not vary between the two viruses, thereby indicating that the N and P proteins are less likely to be associated with the steepened gradient. Instead, this suggests a possible role for the large polymerase protein in decreasing transcription.Whilst this research has not yet identified specific molecular sequences responsible for the minimal pathogenicity of the Meredith/02 virus despite its virulent fusion protein cleavage site, it has focused the investigation on components of the viral replication complex.Therefore directions for further research include investigating the role of the replication complex, in particular, the large polymerase (L) gene in the pathogenicity of Australian NDVs. This could also incorporate further work on the individual proteins via the use of minigenome assays, or by utilising reverse genetics and full-length virus clones.

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Chicken interferons, their receptors and interferon-stimulated genes

Cited by 52 publications

References 117 publications

Intronless and intron-containing type I IFN genes coexist in amphibian Xenopus tropicalis : Insights into the origin and evolution of type I IFNs in vertebrates

Intronless and intron-containing type I IFN genes coexist in amphibian Xenopus tropicalis : Insights into the origin and evolution of type I IFNs in vertebrates

Molecular Evolution of the Porcine Type I Interferon Family: Subtype-Specific Expression and Antiviral Activity

The molecular basis of the pathogenicity of Newcastle disease virus in chickens

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