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Please join use for PhD Student, Jonathan Felix’s Literature Mastery Presentation.
The SARS-CoV-2 pandemic elicited an intense response from all sectors of biotechnology, culminating in rapid development of vaccines and therapeutics for treatment of COVID-19. Although the response to the pandemic set record speeds for vaccine and therapeutic drug development, emerging mutational variants of the SARS-CoV-2 virus have left us searching for more effective and strategic means of combating an ever-mutating pathogen. Evolution of a virus that results in a host immune system’s inability to recognize and neutralize the pathogen is referred to as immune escape. Understanding of potential immune escape mechanisms is a key problem to solve in the development of effective therapeutics in the future. Several approaches taken to understand the structural basis of the interaction between the SARS-CoV-2 spike protein’s receptor binding domain and the ACE-2 receptor show which amino acid residues are necessary for infection of host cells. However, as mutations of interest arise in novel variants such as SARS-CoV-2 Omicron, immune escape occurs. If mutations in amino acid residues necessary for interaction with the ACE-2 receptor have led to immune evasion of the Omicron strain of SARS-CoV-2, could deep mutational profiling of these residues allow for prediction of future variants?
Date: December 5, 2022
Time: 1:00 – 2:00 p.m.
Location: 535 Bldg. – 109 Classroom and Via Zoom (See Outlook invite for Zoom Link)