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A Metagenomics Analysis of Pandemic 2009 H1N1 Infection in Patients in North America

ABSTRACT: The Virochip microarray (version 4.0) was used to detect viruses in patients from North America with unexplained influenza-like illness at the onset of the 2009 H1N1 pandemic. We used metagenomics-based technologies (the Virochip microarray) and deep sequencing to analyze nasal swab samples from individuals with 2009 H1N1 infection. This Series includes the Virochip microarray data only.

ORGANISM(S): Homo sapiens

SUBMITTER: Charles Chiu

PROVIDER: E-GEOD-24034 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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A Metagenomics Analysis of Pandemic 2009 H1N1 Infection in Patients in North America

Project description:The Virochip microarray (version 4.0) was used to detect viruses in patients from North America with unexplained influenza-like illness at the onset of the 2009 H1N1 pandemic.

2010-11-01 | GSE24034 | GEO

Pandemic Swine-Origin H1N1 Influenza A Virus Isolates Show Heterogeneous Virulence in Macaques

Project description:This study used virological, histological, immunological and global gene expression to compare the virlence of two newly emerged 2009 H1N1 isolates (A/Mexico/InDRE4487/2009 and A/Mexico/4108/2009) and current seasonal H1N1 influenza strain (A/Kawasaki/UTK-4/2009) in experimentally infected cynomolgus macaques. We showed that infection of macaques with two genetically similar but clinically distinct SOIV isolates from the early stage of the pandemic (A/Mexico/4108/2009 and A/Mexico/InDRE4487/2009) resulted in upper and lower respiratory tract infections and clinical disease ranging from mild to severe pneumonia. Disease associated with these SOIV isolates was clearly advanced over the mild infection caused by A/Kawasaki/UTK-4/2009, a current seasonal strain.

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Role of Interleukin-6 in Influenza Pandemic A (H1N1pdm) Infection in Mice

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2012-06-25 | GSE31022 | GEO

Differential microRNA expression profiles of mouse lungs infected with 2009 pandemic H1N1 influenza virus and seasonal H1N1 virus

Project description:To further understand the molecular pathogenesis of the 2009 pandemic H1N1 influenza virus infection, we profiled cellular miRNAs of lung tissue from BALB/c mice infected with influenza virus BJ501 and a mouse-adapted influenza virus A/Puerto Rico/8/34 (H1N1)(PR8) as a comparison.

2013-04-17 | GSE46087 | GEO

Comparative transcriptomic analysis of acute host responses during 2009 pandemic H1N1 influenza infection in mouse, macaque, and swine

Project description:This SuperSeries is composed of the following subset Series: GSE35738: 2009 pandemic H1N1 virus causes disease and upregulation of genes related to inflammatory and immune response, cell death, and lipid metabolism in pigs GSE40088: Comparative transcriptomic analysis of acute host responses during 2009 pandemic H1N1 influenza infection in mouse, macaque, and swine (macaque dataset) GSE40091: Comparative transcriptomic analysis of acute host responses during 2009 pandemic H1N1 influenza infection in mouse, macaque, and swine (mouse dataset) Refer to individual Series

2012-08-13 | E-GEOD-40092 | biostudies-arrayexpress

Human Calu-3 cell transcriptome response to wild-type pandemic H1N1 (A/California/04/2009), natural isolate

Project description:The purpose is to obtain samples for mRNA, miRNA, proteomics, lipidomics, metabolomics, and histopathology analysis in human Calu-3 cells infected with wild-type pandemic H1N1 (A/California/04/2009), natural isolate.

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Human Calu-3 cell transcriptome response to wild-type pandemic H1N1 (A/California/04/2009), natural isolate [mRNA]

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Pandemic Swine-Origin H1N1 Influenza A Virus Isolates Show Heterogeneous Virulence in Macaques

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IM002, IM009 - Implication of inflammatory macrophages, nuclear receptors and interferon regulatory factors in increased virulence of pandemic 2009 H1N1 influenza A virus after host adaptation

Project description: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. Here, we compared the gene-expression response following infection of mice with A/CA/04/2009 (CA/04) or the virulent mouse-adapted strain (MA-CA/04). Microarray analysis revealed that increased pathogenicity of MA-CA/04 was associated with: (1) early and sustained inflammatory and interferon response that could be driven in part by interferon regulatory factors (IRFs) and increased NF-kappaB activation, as well as inhibition of the negative regulator TRIM24, (2) early and persistent infiltration of immune cells, including inflammatory macrophages, and (3) the absence of activation of lipid metabolism later in infection, that may be mediated by nuclear receptors inhibition, including PPARG, HNF1A and 4A, with pro-inflammatory consequences. Further investigation of these signatures in the host response to other H1N1 viruses of varied pathogenicity confirmed their general relevance for virulence of influenza virus and suggested that lung response to MA-CA/04 virus was similar to that following lethal H1N1 r1918 influenza virus. This study links for the first time differential activation of IRFs, nuclear receptors, and macrophage infiltration with influenza virulence in vivo.

2012-03-08 | GSE36328 | GEO

A positive feedback-loop regulates transcriptional response to murine pandemic influenza infection

Project description:The biological basis for the increased severity of influenza A viruses during the 2009 influenza pandemic remains unclear. Intra-host evolution of quasispecies and strong inflammation were identified as important hallmarks of severe pandemic H1N1 influenza A virus 2009 (A(H1N1)pdm09) infection. HA-222D/G quasispecies of A(H1N1)pdm09 were shown to undergo fast evolution and to cause severe influenza in human and mice. Here, we analysed the whole genome transcriptional response of mice infected with the A/Jena/5258/09 (mpJena/5258) virus over a period of 12 days to gain insights into the pathogenesis of A(H1N1)pdm09 HA-222D/G quasispecies on a molecular level. Remarkably, the transcriptional response to severe mpJena/5258 showed biphasic expression profile for the majority of genes which was never shown before. The gene expression analysis shows first peak with 968 differentially expressed genes at day 2 post infection (p.i.), followed by a stagnant recovery phase with 359 differentially expressed genes at day 4 p.i., and a second peak with 1001 differentially expressed genes at day 7 p.i., finally followed by a recovery phase. Using a reverse engineering strategy, a regulatory network was inferred to identify key interactions leading to severe pathogenesis of mpJena/5258. Known regulatory interactions were extracted by Pathway Studio 9.0 and softly integrated during network inference. The results demonstrate a hyper-responsive action and a positive feedback loop of IFN gamma (Ifng), Stat1 and Tlr3 signalling during mpJena/5258 infection. In conclusion, mpJena/5258 infection is associated with biphasic gene expression profile and a positive feedback mechanism of Ifng which correlates with the evolution of HA-222D/G quasispecies and leads to overwhelming immune response. A significant correlation were found between the co-expression action of three genes (Ifng, Stat1 and Tlr3) with a phenomenological clinical symptom score.

2017-02-10 | GSE67241 | GEO

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