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Expression data of lungs from chickens infected with different H5N1 Avian Influenza Viruses

ABSTRACT: This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

ORGANISM(S): Gallus gallus

SUBMITTER: Jiao Hu

PROVIDER: E-GEOD-53932 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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PA-X decreases the pathogenicity of highly pathogenic H5N1 influenza A virus in avian species by inhibiting virus replication and host response.

Hu Jiao J Mo Yiqun Y Wang Xiaoquan X Gu Min M Hu Zenglei Z Zhong Lei L Wu Qiwen Q Hao Xiaoli X Hu Shunlin S Liu Wenbo W Liu Huimou H Liu Xiaowen X Liu Xiufan X

Journal of virology 20150128 8

<h4>Unlabelled</h4>PA-X is a newly discovered protein that decreases the virulence of the 1918 H1N1 virus in a mouse model. However, the role of PA-X in the pathogenesis of highly pathogenic avian influenza viruses (HPAIV) of the H5N1 subtype in avian species is totally unknown. By generating two PA-X-deficient viruses and evaluating their virulence in different animal models, we show here that PA-X diminishes the virulence of the HPAIV H5N1 strain A/Chicken/Jiangsu/k0402/2010 (CK10) in mice, ch ...[more]

PMID: 25631083

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Expression data of lungs from chickens infected with different H5N1 Avian Influenza Viruses [12 hours post infection]

Project description:Recently, a novel protein in the influenza virus segment 3 has been identified, namely PA-X. This small protein has been reported to play a role in modulating host response of the 1918 H1N1 pandemic virus-infected mice. However, poteinal role of this protein in the pathogenicity and regulating host response of the highly pathogenic H5N1 virus in a chicken animal model is completely unknown. We used microarray analysis to evaluate the global transcriptional response in the lungs of the chickens infected with the parental strain (CK10) and PA-X deficiency mutant strain (CK-PAX3). Chickens were inoculated with CK10 or CK-PAX3 or mock-infected. At 12 hours post infection, lungs were isolated from three chickens per group for RNA extraction and hybridization on Affymetrix microarrays. Samples were named as follows: CK10 (CK10-1,CK10-2,CK10-3), CK-PAX3 (CK-PAX3-1,CK-PAX3-2, CK-PAX3-3), Control (C-1, C-2, C-3).

2015-03-04 | E-GEOD-53930 | biostudies-arrayexpress

Expression data of lungs from chickens infected with different H5N1 Avian Influenza Viruses [24 hours post infection]

Project description:Recently, a novel protein in the influenza virus segment 3 has been identified, namely PA-X. This small protein has been reported to play a role in modulating host response of the 1918 H1N1 pandemic virus-infected mice. However, poteinal role of this protein in the pathogenicity and regulating host response of the highly pathogenic H5N1 virus in a chicken animal model is completely unknown. We used microarray analysis to evaluate the global transcriptional response in the lungs of the chickens infected with the parental strain (CK10) and PA-X deficiency mutant strain (CK-PAX3). Chickens were inoculated with CK10 or CK-PAX3 or mock-infected. At 24 hours post infection, lungs were isolated from three chickens per group for RNA extraction and hybridization on Affymetrix microarrays. Samples were named as follows: CK10 (CK10-1,CK10-2,CK10-3), CK-PAX3 (CK-PAX3-1,CK-PAX3-2, CK-PAX3-3), Control (C-1, C-2, C-3).

2015-03-04 | E-GEOD-53931 | biostudies-arrayexpress

Expression data of lungs from chickens infected with different H5N1 Avian Influenza Viruses

Project description:This SuperSeries is composed of the SubSeries listed below.

2015-03-04 | GSE53932 | GEO

Expression data of lungs from chickens infected with different H5N1 Avian Influenza Viruses [24 hours post infection]

2015-03-04 | GSE53931 | GEO

Expression data of lungs from chickens infected with different H5N1 Avian Influenza Viruses [12 hours post infection]

2015-03-04 | GSE53930 | GEO

Phylogeny, Pathogenicity, and Transmission of H5N1 Avian Influenza Viruses in Chickens.

Project description:We analyzed five H5N1 avian influenza viruses (AIVs) isolated from different birds in 2012 in China. Based on whole-genome sequences, we divided the viruses into four genotypes. The DKE26, GSE43, and DKE53 viruses belonged to Genotypes 1-3, respectively. The CKE93 and CKE96 viruses were classified into Genotype 4. Genotypes 1-3 correspond to the viruses containing the HA gene of clade 2.3.2, and Genotype 4 is the virus that bears the HA gene of clade 7.2. To better understand the pathogenicity and transmission of the viruses, we infected chickens with 103 EID50/0.1 ml GSE43 (clade 2.3.2) or CKE93 (clade 7.2) virus. Our results revealed that 6 of 7 specific-pathogen-free (SPF) chickens inoculated with GSE43 virus were dead before 7-day post-infection, but all the SPF chickens inoculated with CKE93 virus survived the infection. Both the GSE43 and CKE93 viruses replicated systemically in chickens. The virus titers of GSE43 virus in tested organs were obviously higher than those of CKE93 virus. Our results revealed that the pathogenicity and replication of GSE43 in chickens was much higher than those of CKE93. The GSE43 virus could transmit between chickens, but the CKE93 could not transmit between chickens by naïve contact. Therefore, different clades of H5N1 AIVs possessed variable pathogenicities and transmission abilities among chickens. Our study contributes to knowledge of pathogenic variations of prevalent H5N1 viruses.

| S-EPMC5515836 | biostudies-literature

RNA-seq data of lungs from mouse infected with different H5N1 Avian Influenza Viruses

Project description:Long non-coding RNAs (lncRNAs) play multiple key regulatory roles in various biological processes. However, their function in influenza A virus (IAV) pathogenicity remains largely unexplored. Here, using next generation sequencing, we systemically compared the whole-transcriptome response of the mouse lung infected either with high-pathogenic (A/Chicken/Jiangsu/k0402/2010, CK10) or with nonpathogenic (A/Goose/Jiangsu/k0403/2010, GS10) H5N1 strains. A total of 370 significantly differentially expressed (DE) lncRNAs from three replicates were identified associated with the high virulence of CK10, whereas the corresponding number for GS10 was 229.

2018-09-06 | GSE100522 | GEO

Expression data of spleens from chickens infected with different Newcastle Disease Viruses

Project description:Genotype VIId NDV is characterized by severe tissue damage in chicken lymphoid organs compared to other virulent strains. However, biological basis of this unusual pathological phenotype is unknown. Host response is associated with pathogenicity of Newcastle Disease Virus (NDV). We aim to determine the contribution of host response to the severe tissue destruction in the lymphoid system caused by genotype VIId NDV. We used microarray analysis to evaluate the global transcriptional response in the spleen of chickens infected with genotype VIId NDV strain JS5/05 and genotype IV NDV Herts/33. Chickens were inoculated with JS5/05 or Herts/33 or mock-infected. At day 2 post infection, spleens were isolated from three chickens per group for RNA extraction and hybridization on Affymetrix microarrays. Samples were named as follows: JS5/05 (I4_1_NS,I4_2_NS,I4_3_NS), Herts/33 (H1_NS,H2_NS, H3_NS), control (C1_NS, C2_NS, C3_NS).

2012-08-14 | E-GEOD-40100 | biostudies-arrayexpress

NP, PB1, and PB2 viral genes contribute to altered replication of H5N1 avian influenza viruses in chickens.

Project description:The virulence determinants for highly pathogenic avian influenza viruses (AIVs) are considered multigenic, although the best characterized virulence factor is the hemagglutinin (HA) cleavage site. The capability of influenza viruses to reassort gene segments is one potential way for new viruses to emerge with different virulence characteristics. To evaluate the role of other gene segments in virulence, we used reverse genetics to generate two H5N1 recombinant viruses with differing pathogenicity in chickens. Single-gene reassortants were used to determine which viral genes contribute to the altered virulence. Exchange of the PB1, PB2, and NP genes impacted replication of the reassortant viruses while also affecting the expression of specific host genes. Disruption of the parental virus' functional polymerase complexes by exchanging PB1 or PB2 genes decreased viral replication in tissues and consequently the pathogenicity of the viruses. In contrast, exchanging the NP gene greatly increased viral replication and expanded tissue tropism, thus resulting in decreased mean death times. Infection with the NP reassortant virus also resulted in the upregulation of gamma interferon and inducible nitric oxide synthase gene expression. In addition to the impact of PB1, PB2, and NP on viral replication, the HA, NS, and M genes also contributed to the pathogenesis of the reassortant viruses. While the pathogenesis of AIVs in chickens is clearly dependent on the interaction of multiple gene products, we have shown that single-gene reassortment events are sufficient to alter the virulence of AIVs in chickens.

| S-EPMC2293025 | biostudies-literature

The NS segment of H5N1 avian influenza viruses (AIV) enhances the virulence of an H7N1 AIV in chickens.

Project description:Some outbreaks involving highly pathogenic avian influenza viruses (HPAIV) of subtypes H5 and H7 were caused by avian-to-human transmissions. In nature, different influenza A viruses can reassort leading to new viruses with new characteristics. We decided to investigate the impact that the NS-segment of H5 HPAIV would have on viral pathogenicity of a classical avian H7 HPAIV in poultry, a natural host. We focussed this study based on our previous work that demonstrated that single reassortment of the NS-segment from an H5 HPAIV into an H7 HPAIV changes the ability of the virus to replicate in mammalian hosts. Our present data show that two different H7-viruses containing an NS-segment from H5-types (FPV NS GD or FPV NS VN) show an overall highly pathogenic phenotype compared with the wild type H7-virus (FPV), as characterized by higher viral shedding and earlier manifestation of clinical signs. Correlating with the latter, higher amounts of IFN-? mRNA were detected in the blood of NS-reassortant infected birds, 48 h post-infection (pi). Although lymphopenia was detected in chickens from all AIV-infected groups, also 48 h pi those animals challenged with NS-reassortant viruses showed an increase of peripheral monocyte/macrophage-like cells expressing high levels of IL-1?, as determined by flow cytometry. Taken together, these findings highlight the importance of the NS-segment in viral pathogenicity which is directly involved in triggering antiviral and pro-inflammatory cytokines found during HPAIV pathogenesis in chickens.

| S-EPMC3922795 | biostudies-literature

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