SARS-CoV-2 Interactions with the Host Innate Immune Response and the Ubiquitin System

Presented at: Coronavirus Series
C.E. Credits: P.A.C.E. CE Florida CE
  • Ricardo Rajsbaum, PhD.

    Associate Professor, Department of Medicine, Director, Center for Virus-Host-Innate Immunity (CVHII), Institute for Infectious and Inflammatory Diseases, Rutgers University, New Jersey Medical School Cancer Center


The host antiviral innate immune response protects the host against infection. Like with other viruses, the host recognizes SARS-CoV-2 infection and triggers a series of signaling cascades that culminate in the production of cytokines and type-I Interferons (IFN-I) that reduce virus spread. To avoid detrimental inflammation, the IFN system is regulated by different molecular processes, including the host ubiquitin system. However, like other viruses, SARS-CoV-2 has developed mechanisms to antagonize both IFN induction and signaling. In this talk we will discuss mechanisms used by SARS-CoV-2 to escape the innate antiviral response, with a focus on interactions with the host ubiquitin system.
Learning objectives:
1. Clarify molecular mechanisms of host innate antiviral immunity that lead to protection against SARS-CoV-2 infection
2. Classify mechanisms of SARS-CoV-2 antagonism of innate immunity and type-I IFN induction
3. Outline mechanisms of virus-host interactions regulated by the host ubiquitin system

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