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Remodelling of the Host Cell RNA Splicing Machinery During an Adenovirus Infection

  • Chapter
Adenoviruses: Model and Vectors in Virus-Host Interactions

Part of the book series: Current Topics in Microbiology and Immunology ((CT MICROBIOLOGY,volume 272))

Abstract

Adenovirus makes extensive use of RNA splicing to produce a complex set of spliced mRNAs during virus replication. All transcription units, except pIX and IVa2, encode multiple alternatively spliced mRNAs. The accumulation of viral mRNAs is subjected to a temporal regulation, a mechanism that ensures that proteins that are needed at certain stages of the viral life cycle are produced. The complex interaction between host cell RNA splicing factors and viral regulatory elements has been studied intensely during the last decade. Such studies have begun to produce a picture of how adenovirus remodels the host cell RNA splicing machinery to orchestrate the shift from the early to the late profile of viral mRNA accumulation. Recent progress has to a large extent focused on the mechanisms regulating E1A and Ll alternative splicing. Here we will review the current knowledge of cis-acting sequence element, trans-acting factors and mechanisms controlling E1A and L1 alternative splicing.

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Authors and Affiliations

  1. Department of Medical Biochemistry and Microbiology, BMC, Uppsala University, 751 23, Uppsala, Sweden

    G. Akusjärvi

  2. Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/INSERM/ULP, 1 Rue Laurent Fries, BP 163, 67404, Illkirch Cedex, France

    J. Stévenin

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  1. Institut für Klinische und Molekulare Virologie, Universität Erlangen-Nürnberg, 91054, Erlangen, Germany

    Walter Doerfler

  2. Institut für Genetik, Universität zu Köln, Weyertal 121, 50931, Köln, Germany

    Petra Böhm

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Akusjärvi, G., Stévenin, J. (2003). Remodelling of the Host Cell RNA Splicing Machinery During an Adenovirus Infection. In: Doerfler, W., Böhm, P. (eds) Adenoviruses: Model and Vectors in Virus-Host Interactions. Current Topics in Microbiology and Immunology, vol 272. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-05597-7_9

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