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SEP 17, 2020 9:00 AM PDT

Coronaviruses: History, Biology and Innate Immune Antagonism

C.E. Credits: P.A.C.E. CE Florida CE
Speaker
  • Professor and Vice Chair Department of Microbiology, Co-Director, Penn Center for Research on Coronaviruses and Other Emerging Pathogens Perelman school of Medicine University of Pennsylvania
    Biography
      Susan Weiss obtained her PhD in Microbiology from Harvard University working on paramyxoviruses and did postdoctoral training in retroviruses at University of California, San Francisco. She is currently Professor and Vice Chair, Department of Microbiology and Co-director of the Penn Center for Research on Coronaviruses and Other Emerging Pathogens at the Perelman School of Medicine at the University of Pennsylvania. She has worked on many aspects of coronavirus replication and pathogenesis over the last forty years, making contributions to understanding the basic biology as well as organ tropism and virulence. She has worked with murine coronavirus (MHV), MERS-CoV and most recently SARS-CoV-2. Her work for the last ten years has focused on coronavirus interaction with the host innate immune response and viral innate antagonists of double-stranded RNA induced antiviral pathways. Her other research interests include activation and antagonism of the antiviral oligoadenylate-ribonuclease L (OAS-RNase L) pathway, flavivirus- primarily Zika- virus-host interactions and pathogenic effects of host endogenous dsRNA.

    Abstract

    Part I:  Introduction and history coronaviruses dating back to the 1980s and coronavirus biology. I will describe the coronavirus life cycle pointing steps that may serve as targets of antiviral therapies that may effective against most if not all coronaviruses.

    Part II. Coronaviruses are highly effective in antagonizing host innate immune responses, more specifically interferon (IFN) induction and signaling pathways. MERS-CoV and SARS-CoV fail to induce IFN early in infections of humans and in mouse models while IFN production in late disease may be pathogenic. Antagonism of host responses is carried out through expression of multiple viral accessory proteins as well as conserved replicase encoded proteins, sometimes with redundant activities. Our lab focuses on the double-stranded RNA induced antiviral pathways: type I and types III IFNs, oligoadenylate synthetase-ribonuclease (OAS-RNase L) and protein kinase R (PKR). Activation of these pathways leads to inhibition of viral replication, shut down of protein synthesis and apoptotic cell death. I will discuss coronavirus antagonism of these pathways using examples from our previous studies of the betacoronaviruses murine coronavirus MHV and MERS-CoV and recent data on SARS-CoV-2.

    Learning Objectives:

    1. Coronaviruses enter cells by two pathways, at the plasma membrane fusion or through endosomes

    2. Coronaviruses encode 16 conserved non-structural proteins in the replicase locus, potential targets for pan coronavirus antivirals

    3. Coronaviruses are adept at antagonizing activation of dsRNA induced antiviral pathways, including interferon signaling, OAS-RNase L and PKR


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