Analysis and Applied Math Seminar
The Analysis and Applied Mathematics (AAM) Seminar is intended for Kennesaw State faculty working in the various areas of analysis and applied mathematics to get together to discuss their current work or related questions. Seminars often involved advanced mathematical knowledge. However, the seminars are open to anyone who is interested in attending.
No events currently scheduled
Friday, November 15, 2019
- Jeremy Harris, Emory University
- "Cellular co-infection increases the rate of influenza A virus production and shapes the immune response to infection"
- TIME/LOCATION: 2:00-3:00pm, D-249, Marietta campus
- ABSTRACT: During viral infection, the number of virions infecting individual cells can vary significantly over time and space. While this variation in the cellular multiplicity of infection (MOI) may have important phenotypic consequences, the relationship between cellular phenotypes (output) in response to viral infection and the cellular MOI (input) remains poorly understood. To study these cellular input/output relationships, our experimental collaborators performed bulk cell culture infection experiments, in which they infected ∼2 million cells with influenza A virus (IAV) at various bulk MOI treatments. They measured several cellular response outcomes during a single round of replication (from 0–18 hours post infection): cell death kinetics, viral infection distribution, virus production, interferon induction, and superinfection exclusion. To determine how these cellular responses change as a result of cellular coinfection, we developed several mathematical models that include single-cell level input/output relationships. Using an appropriate viral infection distribution across cells, we can 'scale' these single-cell relationships up to the bulk cell culture level. By fitting these models to the bulk cell culture data, we were able to determine which infection outcomes were sensitive to cellular coinfection. For instance, we found that virus production increases and saturates at high levels of viral input. We also found that infected cell death rates and type I interferon expression are independent of viral input while type III interferon induction is sensitive to viral input, identifying a role for cellular co-infection in shaping the host immune response to IAV infection. Our results suggest that, the extent of cellular co-infection by influenza viruses may play a critical role in determining viral fitnesses, cellular response phenotypes, and overall infection outcomes during the viral infection.
Friday, November 8, 2019
- Lingju Kong, University of Tennessee at Chattanooga
Friday, September 20, 2019
- Sara Motlaghian, Georgia State University
Friday, October 11, 2019