Dynamic oscillation of translation and stress granule formation mark the cellular response to virus infection

Alessia Ruggieri; Eva Dazert; Philippe Metz; Sarah Hofmann; Jan-Philip Bergeest; Johanna Mazur; Peter Bankhead; Marie-Sophie Hiet; Stephanie Kallis; Gualtiero Alvisi; Charles Samuel; Volker Lohmann; Lars Kaderali; Karl Rohr; Michael Frese; Georg Stoecklin; Ralf Bartenschlager

doi:10.1016/J.CHOM.2012.05.013

Dynamic oscillation of translation and stress granule formation mark the cellular response to virus infection

Alessia Ruggieri, Eva Dazert, Philippe Metz, Sarah Hofmann, Jan-Philip Bergeest, Johanna Mazur, Peter Bankhead, Marie-Sophie Hiet, Stephanie Kallis, Gualtiero Alvisi, Charles Samuel, Volker Lohmann, Lars Kaderali, Karl Rohr, Michael Frese, Georg Stoecklin, Ralf Bartenschlager

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Abstract

Virus infection-induced global protein synthesis suppression is linked to assembly of stress granules (SGs), cytosolic aggregates of stalled translation preinitiation complexes. To study long-term stress responses, we developed an imaging approach for extended observation and analysis of SG dynamics during persistent hepatitis C virus (HCV) infection. In combination with type 1 interferon, HCV infection induces highly dynamic assembly/disassembly of cytoplasmic SGs, concomitant with phases of active and stalled translation, delayed cell division, and prolonged cell survival. Double-stranded RNA (dsRNA), independent of viral replication, is sufficient to trigger these oscillations. Translation initiation factor elF2 alpha phosphorylation by protein kinase R mediates SG formation and translation arrest. This is antagonized by the upregulation of GADD34, the regulatory subunit of protein phosphatase 1 dephosphorylating elF2 alpha. Stress response oscillation is a general mechanism to prevent long-lasting translation repression and a conserved host cell reaction to multiple RNA viruses, which HCV may exploit to establish persistence

Original language	English
Pages (from-to)	71-85
Number of pages	15
Journal	Cell Host Microbe
Volume	12
Issue number	1
DOIs	https://doi.org/10.1016/J.CHOM.2012.05.013
Publication status	Published - 2012

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Ruggieri, A., Dazert, E., Metz, P., Hofmann, S., Bergeest, J-P., Mazur, J., Bankhead, P., Hiet, M-S., Kallis, S., Alvisi, G., Samuel, C., Lohmann, V., Kaderali, L., Rohr, K., Frese, M., Stoecklin, G., & Bartenschlager, R. (2012). Dynamic oscillation of translation and stress granule formation mark the cellular response to virus infection. Cell Host Microbe, 12(1), 71-85. https://doi.org/10.1016/J.CHOM.2012.05.013

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title = "Dynamic oscillation of translation and stress granule formation mark the cellular response to virus infection",

abstract = "Virus infection-induced global protein synthesis suppression is linked to assembly of stress granules (SGs), cytosolic aggregates of stalled translation preinitiation complexes. To study long-term stress responses, we developed an imaging approach for extended observation and analysis of SG dynamics during persistent hepatitis C virus (HCV) infection. In combination with type 1 interferon, HCV infection induces highly dynamic assembly/disassembly of cytoplasmic SGs, concomitant with phases of active and stalled translation, delayed cell division, and prolonged cell survival. Double-stranded RNA (dsRNA), independent of viral replication, is sufficient to trigger these oscillations. Translation initiation factor elF2 alpha phosphorylation by protein kinase R mediates SG formation and translation arrest. This is antagonized by the upregulation of GADD34, the regulatory subunit of protein phosphatase 1 dephosphorylating elF2 alpha. Stress response oscillation is a general mechanism to prevent long-lasting translation repression and a conserved host cell reaction to multiple RNA viruses, which HCV may exploit to establish persistence",

keywords = "Hepatitis C virus, Protein translation, Interferon",

author = "Alessia Ruggieri and Eva Dazert and Philippe Metz and Sarah Hofmann and Jan-Philip Bergeest and Johanna Mazur and Peter Bankhead and Marie-Sophie Hiet and Stephanie Kallis and Gualtiero Alvisi and Charles Samuel and Volker Lohmann and Lars Kaderali and Karl Rohr and Michael Frese and Georg Stoecklin and Ralf Bartenschlager",

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Ruggieri, A, Dazert, E, Metz, P, Hofmann, S, Bergeest, J-P, Mazur, J, Bankhead, P, Hiet, M-S, Kallis, S, Alvisi, G, Samuel, C, Lohmann, V, Kaderali, L, Rohr, K, Frese, M, Stoecklin, G & Bartenschlager, R 2012, 'Dynamic oscillation of translation and stress granule formation mark the cellular response to virus infection', Cell Host Microbe, vol. 12, no. 1, pp. 71-85. https://doi.org/10.1016/J.CHOM.2012.05.013

TY - JOUR

T1 - Dynamic oscillation of translation and stress granule formation mark the cellular response to virus infection

AU - Ruggieri, Alessia

AU - Dazert, Eva

AU - Metz, Philippe

AU - Hofmann, Sarah

AU - Bergeest, Jan-Philip

AU - Mazur, Johanna

AU - Bankhead, Peter

AU - Hiet, Marie-Sophie

AU - Kallis, Stephanie

AU - Alvisi, Gualtiero

AU - Samuel, Charles

AU - Lohmann, Volker

AU - Kaderali, Lars

AU - Rohr, Karl

AU - Frese, Michael

AU - Stoecklin, Georg

AU - Bartenschlager, Ralf

PY - 2012

Y1 - 2012

N2 - Virus infection-induced global protein synthesis suppression is linked to assembly of stress granules (SGs), cytosolic aggregates of stalled translation preinitiation complexes. To study long-term stress responses, we developed an imaging approach for extended observation and analysis of SG dynamics during persistent hepatitis C virus (HCV) infection. In combination with type 1 interferon, HCV infection induces highly dynamic assembly/disassembly of cytoplasmic SGs, concomitant with phases of active and stalled translation, delayed cell division, and prolonged cell survival. Double-stranded RNA (dsRNA), independent of viral replication, is sufficient to trigger these oscillations. Translation initiation factor elF2 alpha phosphorylation by protein kinase R mediates SG formation and translation arrest. This is antagonized by the upregulation of GADD34, the regulatory subunit of protein phosphatase 1 dephosphorylating elF2 alpha. Stress response oscillation is a general mechanism to prevent long-lasting translation repression and a conserved host cell reaction to multiple RNA viruses, which HCV may exploit to establish persistence

AB - Virus infection-induced global protein synthesis suppression is linked to assembly of stress granules (SGs), cytosolic aggregates of stalled translation preinitiation complexes. To study long-term stress responses, we developed an imaging approach for extended observation and analysis of SG dynamics during persistent hepatitis C virus (HCV) infection. In combination with type 1 interferon, HCV infection induces highly dynamic assembly/disassembly of cytoplasmic SGs, concomitant with phases of active and stalled translation, delayed cell division, and prolonged cell survival. Double-stranded RNA (dsRNA), independent of viral replication, is sufficient to trigger these oscillations. Translation initiation factor elF2 alpha phosphorylation by protein kinase R mediates SG formation and translation arrest. This is antagonized by the upregulation of GADD34, the regulatory subunit of protein phosphatase 1 dephosphorylating elF2 alpha. Stress response oscillation is a general mechanism to prevent long-lasting translation repression and a conserved host cell reaction to multiple RNA viruses, which HCV may exploit to establish persistence

KW - Hepatitis C virus

KW - Protein translation

KW - Interferon

U2 - 10.1016/J.CHOM.2012.05.013

DO - 10.1016/J.CHOM.2012.05.013

M3 - Article

SN - 1931-3128

VL - 12

SP - 71

EP - 85

JO - Cell Host Microbe

JF - Cell Host Microbe

IS - 1

ER -

Dynamic oscillation of translation and stress granule formation mark the cellular response to virus infection

Abstract

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