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Influenza A virus induced proteome changes

ABSTRACT: Seasonal epidemics of influenza A virus in the human population are a major cause of severe illness and are of high socio-economic relevance. For the design of effective anti-viral therapies, a detailed knowledge of cellular pathways perturbed by virus infection is critical. We performed comprehensive expression and organellar proteomics experiments using A549, Calu-1 and NCI-H1299 cells to identify new protein targets and cellular pathways affected by influenza A virus.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human) Influenza A Virus (a/aichi/68/2007(h3n2))

TISSUE(S): Epithelial Cell, Cell Culture

DISEASE(S): Influenza

SUBMITTER: Joern Dengjel

LAB HEAD: Joern Dengjel

PROVIDER: PXD009924 | Pride | 2018-07-12

REPOSITORIES: Pride

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			Action	DRS
	20180223_A549_C_1_1.raw	Raw
	20180223_A549_C_1_10.raw	Raw
	20180223_A549_C_1_2.raw	Raw
	20180223_A549_C_1_3.raw	Raw
	20180223_A549_C_1_4.raw	Raw

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Publications

Influenza A Virus Induces Autophagosomal Targeting of Ribosomal Proteins.

Becker Andrea C AC Gannagé Monique M Giese Sebastian S Hu Zehan Z Abou-Eid Shadi S Roubaty Carole C Paul Petra P Bühler Lea L Gretzmeier Christine C Dumit Veronica I VI Kaeser-Pebernard Stéphanie S Schwemmle Martin M Münz Christian C Dengjel Jörn J

Molecular & cellular proteomics : MCP 20180706 10

Seasonal epidemics of influenza A virus are a major cause of severe illness and are of high socio-economic relevance. For the design of effective antiviral therapies, a detailed knowledge of pathways perturbed by virus infection is critical. We performed comprehensive expression and organellar proteomics experiments to study the cellular consequences of influenza A virus infection using three human epithelial cell lines derived from human lung carcinomas: A549, Calu-1 and NCI-H1299. As a common ...[more]

PMID: 29980615

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Influenza A virus induces autophagosomal targeting of ribosomal proteins

Project description:Seasonal epidemics of influenza A virus are a major cause of severe illness and are of high socio-economic relevance. For the design of effective anti-viral therapies, a detailed knowledge of cellular pathways perturbed by virus infection is critical. We performed comprehensive expression and organellar proteomics experiments to identify new protein targets and cellular pathways affected by influenza A virus. Type I as well as type II interferon pathways were upregulated upon infection, affecting amongst others poly ADP-ribose polymerase transcription factors and ubiquitin-like modifiers. In addition, influenza A virus had a major influence on the subcellular localization of proteins and complexes. The vesicular compartment appeared expanded upon infection and in particular the composition of autophagsomes was altered, virus infection leading to targeting of ribosomes to autophagosomes.

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Host Regulatory Network Response in Calu-3 cell Infection with A/CA/04/2009 Influenza virus

Project description:Differential Expression was determined in Calu-3 cells between mock infected and infection with A/CA/04/2009 Influenza virus at nime time points post infection. Calu-3 cells were infected with A/CA/04/2009 Influenza virus at MOI of 3, samples were collected 0,3,7,12,18, 24, 30, 36 and 48 hpi. Expression profiles and DE genes were determined for all time points. There are 3 mock and infected replicates for each time point.

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RNA-Seq of influenza A/Puerto Rico/8/1934 (H1N1) virus infected MRC5, WI-38 VA-13, A549 and HEK293FT human cells

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