VUMC Main Calendar Events

  • 4/25/2017
    11:00 am - 12:00 pm
    Coronavirus-encoded phosphodiesterases that antagonize antiviral innate immunity

    Susan R. Weiss, PhD

    Professor of Microbiology, Associate Dean for Postdoctoral Research Training, Director of Biomedical Postdoctoral Programs, Perelman School of Medicine, University of Pennsylvania

    Coronavirus-encoded phosphodiesterases that antagonize antiviral innate immunity

    The oligoadenylate-ribonuclease L (OAS-RNase L) system is a potent antiviral pathway that leads to degradation of host and viral RNA, inhibition of protein synthesis and downstream apoptosis and inflammation. As such, many viruses encode proteins which allow them to evade this pathway. Some Betacoronaviruses (including murine coronavirus MHV and MERS-CoV) encode phosphodiesterases (PDEs) that degrade 2-5A, the inducer of RNase L. The PDE of MHV is required for antagonism of RNase L, replication in the liver and the induction of hepatitis. The MERS-CoV PDE is unique among viral PDEs in that it has expanded substrate utilization and is expressed primarily in the nucleus. Thus, in addition to its RNase L antagonist activity, the MERS PDE has one or more nuclear activities, including antagonizing expression of interferon lambda and some interferon stimulated genes. Finally the OAS-RNase L pathway can be activated by endogenous dsRNA as well as viral dsRNA, and is a dominant pathway leading to apoptosis. Thus viral antagonism of RNase L both protects the viral genome from degradation and delays cell death, which may lead to further viral spread.

    Infection, Inflammation & Immunity Frontiers Seminar Series

    Sponsored by: Vanderbilt Centers for Immunobiology, Microbial Pathogenesis, Vanderbilt Vaccine Center, Medicine Divisions of Rheumatology, Pediatric Infectious Diseases, and Infectious Diseases

    Contact: Eve Stephens

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