IMAG/MSM WG Multiscale Modeling and Viral Pandemics Zoom
To join the meeting:
Please feel free to forward this invitation on to anyone you think would be interested.
Thursday Nov 18 at 3PM (EST)
The schedule for this week consists of two presentations:
- Christian Forst, Icahn School of Medicine at Mount Sinai. Title: The interplay between the human microbiome and respiratory viruses: A multi scale story of influenza and COVID-19. Abstract: The ongoing SARS-CoV-2 pandemic poses a threat to public health and economy, thus urges the scientific community to join efforts in the search of cures. Meanwhile, both influenza and COVID-19 are respiratory diseases caused by airborne RNA viruses. Microbes in the respiratory system have been proven to contribute to the outcome of the diseases. However, scientific advances from studying influenza infection have potentials to benefit the search of cure for SARS-CoV-2 infections. Here we present a comprehensive, multi-scale network analysis of the systems response to the virus. We have developed methods that integrate single-cell and bulk transcriptomic data. These integrated data were further related to the microbiome and clinical outcomes. By this approach we were able to identify cell-population specific key-regulators and host-processes that are hijacked by the virus for its advantage and that contribute to the severity of these infectious diseases.
- Elebeoba E. May, University of Houston. Title: Model-based Investigation of the Proinflammatory Microenvironment and Response to Gram-negative Bacteria. Abstract: Intracellular pathogens like Francisella tularensis (Ft), a gram-negative Class A biothreat agent can trigger the release of cytokines, chemokines, and effector molecules into the microenvironment surrounding the infected cell, contributing to the formation of a proinflammatory microenvironment (PME). Immune cells recruited into the PME can be primed and activated by cytokine exposure promoting a more robust interaction between infiltrating immune cells and infected cells or, in the case of phagocytic cells, priming the cell to more effectively eliminate subsequent Ft infection. Macrophages and NK cells are central to the innate immune response to Ft and primary producers of TNF-α and IFN-γ, respective. Focusing on these key PME cytokines, which are found to modulate the in vivo response to Ft, we developed in silico and in vitro models to investigate the role of PME in macrophage activation and outcome of infection.
After the presentations we will have breakout rooms for each of the speakers where you may discuss technical questions.