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Highly Pathogenic Avian Influenza Viruses Avoid Effective Inflammatory Response of Human Macrophages

ABSTRACT: 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. Macrophages were infected with low (PR8) and high pathogenic influenza viruses (FPV and H5N1)

ORGANISM(S): Homo sapiens

SUBMITTER: Dorothee Viemann

PROVIDER: E-GEOD-27702 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Highly pathogenic avian influenza viruses inhibit effective immune responses of human blood-derived macrophages.

Friesenhagen Judith J Boergeling Yvonne Y Hrincius Eike E Ludwig Stephan S Roth Johannes J Viemann Dorothee D

Journal of leukocyte biology 20120321 1

Systemic infections with HPAIVs, such as H5N1, are characterized by cytokine burst and sepsis. We investigated the role of human monocyte-derived macrophages in these events after infection with different influenza virus strains. Macrophages were infected with low pathogenic H1N1 (PR8) or high pathogenic H7N7 (FPV) and H5N1 (KAN-1) subtypes. Macrophages were found to be nonpermissive for influenza virus propagation. Surprisingly, transcriptome analysis revealed an insufficient innate immune resp ...[more]

PMID: 22442495

Similar Datasets

Highly Pathogenic Avian Influenza Viruses Avoid Effective Inflammatory Response of Human Macrophages

Project description: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.

2012-05-29 | GSE27702 | GEO

Highly pathogenic influenza virus inhibit Inflammatory Responses in Monocytes via Activation of the Rar-Related Orphan Receptor Alpha (RORalpa)

Project description:Highly pathogenic influenza virus inhibit Inflammatory Responses in Monocytes via Activation of the Rar-Related Orphan Receptor Alpha (RORalpha). Low (PR8) and high pathogenic influenza viruses (FPV and H5N1) were used. Monocytes were infected with low (PR8) and high pathogenic influenza viruses (FPV and H5N1)

2013-07-01 | E-GEOD-35283 | biostudies-arrayexpress

Highly pathogenic influenza virus inhibit Inflammatory Responses in Monocytes via Activation of the Rar-Related Orphan Receptor Alpha (RORalpa)

2013-07-01 | GSE35283 | GEO

Genome wide host gene expression analysis in chicken lungs infected with avian influenza viruses

Project description:The mechanisms responsible for the molecular pathogenesis of the highly pathogenic avian influenza virus (HPAIV) or low pathogenic avian influenza virus (LPAIV) in avian species remain poorly understood. Thus, global immune response of chickens infected with HPAIV H5N1 (A/duck/India/02CA10/2011) and LPAIV H9N2 (A/duck/India/249800/2010) viruses was studied using microarray to identify crucial host genetic components responsive to these infection. HPAIV H5N1 induced excessive mRNA expression of cytokines (IFNA, OASL, MX1, RSAD2, IFITM5, GBP 1, IL1B, IL18, IL22, IL13, IL12B, CCL4, CCL9, CCL10, CX3CL1 etc) in lung tissues. This excessive cytokine response (cytokine storms) may cause tissue damage and high mortality in chickens. In contrast, the expression levels of most of the cytokines remained unchanged in the lungs of LPAIV H9N2 virus infected chickens. This study indicated the relationship between host cytokines response and their roles in pathogenesis in chickens infected with HPAIVs.

2016-01-02 | GSE65231 | GEO

Genome wide host gene expression analysis in chicken lungs infected with avian influenza viruses

2016-07-04 | E-GEOD-65231 | biostudies-arrayexpress

Expression data of influenza A infected human macrophages

2009-10-31 | GSE18816 | GEO

Expression data of influenza A infected human macrophages

Project description:Human disease caused by highly pathogenic avian influenza (HPAI) H5N1 can lead to a rapidly progressive viral pneumonia leading to acute respiratory distress syndrome. There is increasing evidence suggests a role for virus-induced cytokine dysregulation in contributing to the pathogenesis of human H5N1 disease. The key target cells for the virus in the lung are the alveolar epithelium and alveolar macrophages, and previous data has shown that compared to seasonal human influenza viruses, equivalent infecting doses of H5N1 viruses markedly up-regulate pro-inflammatory cytokines in both primary cell types in vitro. The dysregulation of H5N1-induced host responses is therefore important for understanding the viral pathogenesis. We used microarrays to analyze and compare the gene expression profiles in primary human macrophages after influenza A virus infection. Peripheral-blood leucocytes were separated from buffy coats of three healthy blood donors and cells were differentiated for 14 days before use. Differentiated macrophages were infected with H1N1 and H5N1 at a multiplicity of infection (MOI) of two. Total RNA was extracted from cells after 1, 3, and 6h post-infection, and gene expression profiling was performed using an Affymetrix Human Gene 1.0 ST microarray platform.

2009-10-31 | E-GEOD-18816 | biostudies-arrayexpress

Lethal dissemination of H5N1 influenza virus is associated with dysregulation of inflammation and lipoxin signaling in a mouse model of infection

Project description:Periodic outbreaks of highly pathogenic avian H5N1 influenza viruses and the current H1N1 pandemic highlight the need for a more detailed understanding of influenza virus pathogenesis. To investigate the host transcriptional response induced by pathogenic influenza viruses, we used a functional-genomics approach to compare gene expression profiles in lungs from wild-type 129S6/SvEv and interferon receptor (IFNR) knockout mice infected with either the fully reconstructed H1N1 1918 pandemic virus (1918) or the highly pathogenic avian H5N1 virus Vietnam/1203/04 (VN/1203).

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Gene expression analysis of chickens (Gallus gallus) infected with recombinant influenza viruses

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2012-03-31 | GSE32378 | GEO

Quantitative proteomic analysis of duck lung tissue during infection of avian influenza

Project description:Ducks and wild aquatic birds are the natural reservoirs of avian influenza viruses. However, the host proteome response that causes disease in vivo during infection by the highly pathogenic avian influenza (HPAI) H5N1 virus is still not well understood. In the present study, we compared the proteome response in Muscovy duck lung tissue during 3 day of infection with either a highly virulent or an avirulent H5N1 virus. During infection, proteins involved in immune response of neutrophils and size of cells were increased markedly in the lung by the virulent strain, while the avirulent strain evoked a distinct response, characterized by an increase in proteins involved in cell movement, maturation of dendritic cells, adhesion of phagocytes, and immune response of macrophages.

2022-08-22 | PXD002719 | Pride

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