A diverse range of gene products are effectors of the type I interferon antiviral response

John W. Schoggins, Sam J. Wilson, Maryline Panis, Mary Y. Murphy, Christopher T. Jones, Paul Bieniasz and Charles M. Rice ()
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John W. Schoggins: Laboratory of Virology and Infectious Disease, Center for the Study of Hepatitis C, The Rockefeller University
Sam J. Wilson: Howard Hughes Medical Institute, Laboratory of Retrovirology, Aaron Diamond AIDS Research Center, The Rockefeller University
Maryline Panis: Laboratory of Virology and Infectious Disease, Center for the Study of Hepatitis C, The Rockefeller University
Mary Y. Murphy: Laboratory of Virology and Infectious Disease, Center for the Study of Hepatitis C, The Rockefeller University
Christopher T. Jones: Laboratory of Virology and Infectious Disease, Center for the Study of Hepatitis C, The Rockefeller University
Paul Bieniasz: Howard Hughes Medical Institute, Laboratory of Retrovirology, Aaron Diamond AIDS Research Center, The Rockefeller University
Charles M. Rice: Laboratory of Virology and Infectious Disease, Center for the Study of Hepatitis C, The Rockefeller University

Nature, 2011, vol. 472, issue 7344, 481-485

Abstract: Antiviral actions of interferon There is growing interest in antiviral interferon-stimulated genes (ISGs), such as IFITM3 and BST2 (also known as tetherin), because of their potential as drug targets. An overexpression screen has been used to assess the impact of several hundred ISGs on the replication of a number of viruses, including HIV-1 and hepatitis C virus. Combinations of validated antiviral ISGs were found to have additive effects and to converge on translational inhibition. Surprisingly, some ISGs actually enhance the replication of certain viruses, underlining the complexity of the response to interferon.

Date: 2011
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DOI: 10.1038/nature09907

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