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