GEO DataSets

(Submitter supplied) The highly pathogenic avian influenza (HPAI) H5N1 viruses continue to circulate in nature and threaten public health. Although several viral determinants and host factors that influence the virulence of HPAI H5N1 viruses in mammals have been identified, the detailed molecular mechanism remains poorly defined and requires further clarification. In our previous studies, we characterized two naturally isolated HPAI H5N1 viruses that had similar viral genomes but differed substantially in their lethality in mice. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL4134

9 Samples

Download data: TXT

(Submitter supplied) We isolated two highly pathogenic H5N1 avian influenza viruses (AIVs) (CK10 and GS10) with similar genetic background but greatly differ in pathogencity in mice. CK10 is highly pathogenic in mice, whereas GS10 is nonpathogenic. However, the host mechanism of this differecne in pathogenicity is unclear. We used microarray analysis to evaluate the global transcriptional response in the lung of mice infected with CK10 or GS10.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL7202

9 Samples

Download data: TXT

(Submitter supplied) The purpose of this experiment was to understand the pathogenic role of individual 1918 genes on the host response to the 1918 pandemic influenza virus. We examined reassortant avian viruses nearly identical to the pandemic 1918 virus (1918-like avian virus) carrying either the 1918 HA or PB2 gene. Both genes enhanced 1918-like avian virus replication, but only the mammalian host adaptation of the 1918-like avian virus through reassortment of the 1918 PB2 led to increased lethality in mice. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL7202

66 Samples

Download data: TXT

(Submitter supplied) Occasional transmission of highly pathogenic avian H5N1 influenza viruses to humans causes severe pneumonia with high mortality. To better understand the mechanisms via which H5N1 viruses induce severe disease in humans, we infected cynomolgus macaques with six different H5N1 strains isolated from human patients and compared their pathogenicity and the global host responses to the virus infection. Although all H5N1 viruses replicated in the respiratory tract, there was substantial heterogeneity in their replicative ability and in the disease severity induced, which ranged from asymptomatic to fatal. more...

Organism:

Macaca mulatta

Type:

Expression profiling by array

Platform:

GPL14569

45 Samples

Download data: TXT

(Submitter supplied) Influenza A virus (IAV) is a human respiratory pathogen that causes yearly global epidemics, and sporadic pandemics due to human adaptation of pathogenic strains. Efficient replication of IAV in different species is, in part, dictated by its ability to exploit the genetic environment of the host cell. To investigate IAV tropism in human cells, we evaluated the replication of IAV strains in a diverse subset of epithelial cell lines. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL20301

8 Samples

Download data: TXT

(Submitter supplied) This study revealed important similarities but also critical differences between the H5N1 and 1918-reassortant viruses, highlighting aspects of the host–pathogen interface caused by highly virulent influenza viruses.

Organism:

Macaca fascicularis; Macaca mulatta

Type:

Expression profiling by array

Platform:

GPL9861

72 Samples

Download data: TXT

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Gallus gallus

Type:

Expression profiling by array

Platform:

GPL3213

18 Samples

Download data: CEL

(Submitter supplied) 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).

Organism:

Gallus gallus

Type:

Expression profiling by array

Platform:

GPL3213

9 Samples

Download data: CEL

(Submitter supplied) 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).

Organism:

Gallus gallus

Type:

Expression profiling by array

Platform:

GPL3213

9 Samples

Download data: CEL

(Submitter supplied) Background. The pathogenesis of influenza A virus subtype H5N1 (hearafter, "H5N1") infection in humans is not completely understood, although hypercytokinemia is thought to play a role. We previously reported that most H5N1 viruses induce high cytokine responses in human macrophages, whereas some H5N1 viruses induce only a low level of cytokine production similar to that induced by seasonal viruses. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL13607

12 Samples

Download data: TXT

(Submitter supplied) The goals of this study are to compare NGS-derived whole transcriptome profiles (RNA-seq) of H5N1 infected A549 cells overexpressing either negative control mimic or miR-324-5p mimic

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL16791

3 Samples

Download data: TXT

(Submitter supplied) Modulating the host response is a promising approach to treating influenza, a virus whose pathogenesis is determined in part by the host response it elicits. Though the pathogenicity of emerging H7N9 influenza virus has been reported in several animal models, these studies have not included a detailed characterization of the host response following infection. To this end, we characterized the transcriptomic response of BALB/c mice infected with H7N9 (A/Anhui/1/2013) virus and compared it to the responses induced by H5N1 (A/Vietnam/1203/2004), H7N7 (A/Netherlands/219/2003) or H1N1 (A/Mexico/4482/2009) viruses. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL7202

68 Samples

Download data: TXT

(Submitter supplied) While pandemic 2009 H1N1 influenza A viruses were responsible for numerous severe infections in humans, these viruses do not typically cause corresponding severe disease in mammalian models. However, the generation of a virulent 2009 H1N1 virus following serial lung passage in mice has allowed for the modeling of human lung pathology in this species. Genetic determinants of mouse-adapted 2009 H1N1 viral pathogenicity have been identified, but the molecular and signaling characteristics of the host response following infection with this adapted virus have not been described. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL7202

64 Samples

Download data: TXT

(Submitter supplied) Incursions of new pathogenic viruses into humans from animal reservoirs are occurring with alarming frequency. The molecular underpinnings of immune recognition, host responses, and pathogenesis in this setting arepoorly understood. We studied pandemic influenza viruses to determine the mechanism by which increasing glycosylation during evolution of surface proteins facilitates diminished pathogenicity in adapted viruses. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL16570

20 Samples

Download data: CEL

(Submitter supplied) Gene transcription effects of mutations in the infuenza virus A/Hong Kong/1/1968(H3N2) nonstructural 1 NS1 gene in infected human A549 (lung epithilium) cells Influenza A/Hong Kong/156/1997(H5N1) virus NS1 gene mutations F103L and M106I both increase IFN antagonism, virulence and cytoplasmic localization but differ in binding to RIG-I and CPSF30 (manuscript submitted to Virology Journal). Human cells were infected with influenza viruses mutants with specific gain of function mutations in the NS1 gene in order to assess the affects of each mutation on host gene expression. more...

Organism:

Homo sapiens; Mus musculus

Type:

Expression profiling by array

Datasets:

GDS4997 GDS4998

Platforms:

GPL6246 GPL6244

36 Samples

Download data: CEL, CHP

Analysis of M1 cells infected with H3N2 influenza isolate A/Hong Kong/1/1968 (HK-wt) or recombinant HK NS1 mutants. NS1 is a multifunctional virulence factor. These results, together with those from GDS4997, provide insight into molecular effects of NS1 mutation on mouse versus human host cells.

Organism:

Mus musculus

Type:

Expression profiling by array, transformed count, 6 infection sets

Platform:

GPL6246

Series:

GSE48200

18 Samples

Download data: CEL, CHP

Analysis of A549 cells infected with H3N2 influenza isolate A/Hong Kong/1/1968 (HK-wt) or recombinant HK NS1 mutants. NS1 is a multifunctional virulence factor. These results, together with those from GDS4998, provide insight into molecular effects of NS1 mutation on human versus mouse host cells.

Organism:

Homo sapiens

Type:

Expression profiling by array, transformed count, 6 infection sets

Platform:

GPL6244

Series:

GSE48200

18 Samples

Download data: CEL, CHP

(Submitter supplied) Over the last decade, more than half of humans infected with highly pathogenic avian influenza (HPAI) H5N1 viruses have died, and yet virus-induced host signaling has yet to be clearly elucidated. Airway epithelia are known to produce inflammatory mediators that contribute to HPAI H5N1-mediated pathogenicity, but a comprehensive analysis of the host response in this cell type is lacking. Here, we leveraged a systems biology method called weighted gene correlation network analysis (WGCNA) to identify and statistically validate signaling sub-networks that define the dynamic transcriptional response of human bronchial epithelial cells after infection with influenza A/Vietnam/1203/2004 (H5N1, VN1203). more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL6480

36 Samples

Download data: TXT

(Submitter supplied) Macrophages were infected with low (PR8) and high pathogenic influenza viruses (FPV and H5N1). To our surprise a genome-wide comparative systems biology approach revealed that in contrast PR8 infections with HPAIV H5N1 and FPV result in a reduced immune response of human macrophages contradicting a primary role of this cell type for the cytokine storm. Our data point to a viral strategy of HPAIV to bypass a major amplifier of the initial local inflammatory response thereby hampering antiviral effector mechanisms and facilitating virus spreading and systemic disease.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL571

12 Samples

Download data: CEL, CHP

(Submitter supplied) An H5N1 virus-encoded microRNA directly targets mammalian poly(rC) binding protein 2 and is a major contributor to H5N1-associated ‘cytokine storm’ and mortality.

Organism:

Homo sapiens

Type:

Non-coding RNA profiling by high throughput sequencing

Platform:

GPL10999

1 Sample

Download data: TXT