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Influenza A Virus Induces Autophagosomal Targeting of Ribosomal Proteins


Becker, Andrea C; Gannagé, Monique; Giese, Sebastian; Hu, Zehan; Abou-Eid, Shadi; Roubaty, Carole; Paul, Petra; Bühler, Lea; Gretzmeier, Christine; Dumit, Veronica I; Kaeser-Pebernard, Stéphanie; Schwemmle, Martin; Münz, Christian; Dengjel, Jörn (2018). Influenza A Virus Induces Autophagosomal Targeting of Ribosomal Proteins. Molecular & Cellular Proteomics, 17(10):1909-1921.

Abstract

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 response, the type I interferon pathway was up-regulated upon infection. Interestingly, influenza A virus infection led to numerous cell line-specific responses affecting both protein abundance as well as subcellular localization. In A549 cells, the vesicular compartment appeared expanded after virus infection. The composition of autophagsomes was altered by targeting of ribosomes, viral mRNA and proteins to these double membrane vesicles. Thus, autophagy may support viral protein translation by promoting the clustering of the respective molecular machinery in autophagosomes in a cell line-dependent manner.

Abstract

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 response, the type I interferon pathway was up-regulated upon infection. Interestingly, influenza A virus infection led to numerous cell line-specific responses affecting both protein abundance as well as subcellular localization. In A549 cells, the vesicular compartment appeared expanded after virus infection. The composition of autophagsomes was altered by targeting of ribosomes, viral mRNA and proteins to these double membrane vesicles. Thus, autophagy may support viral protein translation by promoting the clustering of the respective molecular machinery in autophagosomes in a cell line-dependent manner.

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Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Institute of Experimental Immunology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Scopus Subject Areas:Physical Sciences > Analytical Chemistry
Life Sciences > Biochemistry
Life Sciences > Molecular Biology
Language:English
Date:October 2018
Deposited On:14 Feb 2019 16:10
Last Modified:29 Jul 2020 09:44
Publisher:American Society for Biochemistry and Molecular Biology
ISSN:1535-9476
OA Status:Hybrid
Free access at:PubMed ID. An embargo period may apply.
Publisher DOI:https://doi.org/10.1074/mcp.RA117.000364
PubMed ID:29980615

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