2′-O methylation of the viral mRNA cap evades host restriction by IFIT family members

Stephane Daffis, Kristy J. Szretter, Jill Schriewer, Jianqing Li, Soonjeon Youn, John Errett, Tsai-Yu Lin, Stewart Schneller, Roland Zust, Hongping Dong, Volker Thiel, Ganes C. Sen, Volker Fensterl, William B. Klimstra, Theodore C. Pierson, R. Mark Buller, Michael Gale, Pei-Yong Shi and Michael S. Diamond ()
Additional contact information
Stephane Daffis: Washington University School of Medicine
Kristy J. Szretter: Washington University School of Medicine
Jill Schriewer: Saint Louis University School of Medicine
Jianqing Li: Washington University School of Medicine
Soonjeon Youn: Washington University School of Medicine
John Errett: University of Washington School of Medicine
Tsai-Yu Lin: Viral Pathogenesis Section, Laboratory of Viral Diseases, National Institutes of Health
Stewart Schneller: Auburn University
Roland Zust: Institute of Immunobiology, Kantonal Hospital St Gallen
Hongping Dong: Wadsworth Center
Volker Thiel: Institute of Immunobiology, Kantonal Hospital St Gallen
Ganes C. Sen: Cleveland Clinic, Lerner Research Institute
Volker Fensterl: Cleveland Clinic, Lerner Research Institute
William B. Klimstra: University of Pittsburgh Medical School
Theodore C. Pierson: Viral Pathogenesis Section, Laboratory of Viral Diseases, National Institutes of Health
R. Mark Buller: Midwest, Pacific Northwest, and Northeast Regional Centers for Biodefense and Emerging Infectious Diseases Research
Michael Gale: Midwest, Pacific Northwest, and Northeast Regional Centers for Biodefense and Emerging Infectious Diseases Research
Pei-Yong Shi: Midwest, Pacific Northwest, and Northeast Regional Centers for Biodefense and Emerging Infectious Diseases Research
Michael S. Diamond: Washington University School of Medicine

Nature, 2010, vol. 468, issue 7322, 452-456

Abstract: Evasion of host antiviral mechanisms Many cellular messenger RNAs and viral RNAs are methylated at the 2′-O position of the 5′ guanosine cap. The role of this modification in virus infection has been unclear. Michael Diamond and colleagues now show that this form of methylation enables several unrelated viruses to evade innate host antiviral responses through escape from suppression by interferon-stimulated genes. This suggests an evolutionary explanation for 2′-O methylation of cellular mRNA: it may distinguish self from non-self RNA under conditions of infection. Novel classes of pharmacological agents that specifically inhibit cytoplasmic viral 2′-O methyltransferases may be expected to have broad-spectrum antiviral activity.

Date: 2010
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DOI: 10.1038/nature09489

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