"Non-canonical functions IRFs in controlling viral inflammation"

Presented by Dr. Saurabh Chattopadhyay, College of Medicine, University of Kentucky.

About Dr. Chattopadhyay's research

Our lab studies host-pathogen interaction, and in this context, we primarily focus on viral pathogens, such as respiratory viruses, which cause significant human diseases and their interactions with the host innate immunity. The innate immune response is the first line of defense against microbial infections, and the type-I interferon system is a key component of cellular antiviral innate immunity.

Virus-infected cells are rapidly detected by pattern recognition receptors, which activate, via a series of intracellular signaling pathways, the transcription factors, IRFs and NF-kB, which are essential for the synthesis of interferons and antiviral genes in the infected cells (part-I). Interferons are cytokines, which get secreted from the infected cells and act on the yet uninfected cells to amplify the antiviral responses by inducing a number of interferon-stimulated genes, many of which encode proteins with antiviral activities (part-II). These responses together not only mount an antiviral state in the acute phase of the infection but also help shape the adaptive immune responses of the host.

We study these transcription factors (IRFs and NF-kB) in great detail for their antiviral functions using engineered cell lines and mouse models. Recent studies from our lab underscore the importance of the crosstalk between these transcription factors and how this regulates the antiviral responses. In addition, we utilize high-throughput genetic and drug screens to identify new genes and drugs that regulate cellular antiviral responses. In summary, we take a combined approach to identify the molecular mechanism of the host-virus interaction and evaluate their relative contribution using appropriate mouse models.