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Adenoviruses: Model and Vectors in Virus-Host Interactions pp 245–288Cite as

E1A-Based Determinants of Oncogenicity in Human Adenovirus Groups A and C

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Part of the book series: Current Topics in Microbiology and Immunology ((CT MICROBIOLOGY,volume 273))

Abstract

A broad spectrum of genetic and molecular investigations carried out with group C, Ad2 and Ad5, and with group A, Ad12, have shown that early regionl (El) gene products are sufficient for complete transformation of rodent cells in vitro by these viruses. During the past quarter century, the processes by which E1A proteins, in cooperation with E1B proteins, perturb the cell cycle and induce the transformed phenotype, have become well defined. Somewhat less understood is the basis for the differential oncogenicity of these two groups of viruses, and the processes by which the E1A proteins of Ad12 induce a tumorigenic phenotype in transformants resulting from infection of cells in vivo and in vitro. In this chapter we review previous findings and present new evidence which demonstrates that Ad12 E1A possesses two or more independent functions enabling it to induce tumors. One of these functions lies in its capacity to repress transcription of MHC class I genes, allowing the tumor cells to avoid lysis by cytotoxic T lymphocytes. We have shown that class I repression is mediated through increased binding of repressor COUP-TF and decreased binding of NF-kB to the class I enhancer. In addition to mediating immune escape, DA also determines the susceptibility of transformants to Natural Killer (NK) cell lysis, and in this case, also, Ad12 transformants are not susceptible. By using Ad 12 mutants containing chimeric E1A Ad12-Ad5 genes, point mutations, or a specific deletion, we have shown that the unique spacer region of Ad12 E1A is an oncogenic determinant, but is not required for transformation in vitro. Given that the E1A regions responsible for class I repression are first exon encoded, we have examined a set of cell lines transformed by these altered viruses, and have found that while they display greatly reduced tumorigenicity, they maintain a wild-type capacity to repress class I transcription. Whether the spacer contributes to NK evasion remains unresolved. Lastly, we discuss the properties of the Ad2/Ad5 E1A C-terminal negative modulator of tumorigenicity, and examine the effects on transformation, tumor induction and transformant tumorigenicity, when the Ad5 negative modulator is placed by chimeric construction in Ad12 E1A.

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Authors and Affiliations

  1. Department of Biological Sciences, Carnegie Mellon University, 4400 Fifth Avenue, Pittsburgh, PA, 15213, USA

    J. F. Williams, Y. Zhang & M. A. Williams

  2. Department of Microbiology, School of Dental Medicine, Department of Biochemistry and Molecular Biophysics, University of Pennsylvania, Philadelphia, PA, 19104, USA

    S. Hou & R. P. Ricciardi

  3. Institute for Molecular Virology, University of Wisconsin, Madison, WI, 53706, USA

    D. Kushner

Authors
  1. J. F. Williams
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  2. Y. Zhang
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  3. M. A. Williams
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  4. S. Hou
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  5. D. Kushner
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  6. R. P. Ricciardi
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Editors and Affiliations

  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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© 2004 Springer-Verlag Berlin Heidelberg

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Williams, J.F., Zhang, Y., Williams, M.A., Hou, S., Kushner, D., Ricciardi, R.P. (2004). E1A-Based Determinants of Oncogenicity in Human Adenovirus Groups A and C. In: Doerfler, W., Böhm, P. (eds) Adenoviruses: Model and Vectors in Virus-Host Interactions. Current Topics in Microbiology and Immunology, vol 273. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-05599-1_8

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  • DOI: https://doi.org/10.1007/978-3-662-05599-1_8

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-05715-1

  • Online ISBN: 978-3-662-05599-1

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