| Gender | Male |
|---|---|
| mark.chua@mssm.edu | |
| Education and Training | Ph.D., McGill University |
| Postdoctoral Fellowship, Harvard University | |
| Awards | 2009 - 2014 Presidential Early Career Award for Scientists and Engineers (PECASE) |
| 2009 - 2010 Doctor Harold and Golden Lamport Award for Excellence in Basic Research |
|
| 2008 - 2012 Young Investigator Award Army Research Office |
|
| 2008 - 2012 Pew Scholar Pew Charitable Funds |
| Education and Training | Ph.D., McGill University |
|---|---|
| Postdoctoral Fellowship, Harvard University |
Specific Clinical/Research Interests: Host-pathogen interactions; virus-induced cell signaling
Current Students: Alissa Pham, Jasmine Perez, Andrew Varble
Postdoctoral Fellows: Sonja Schmid
Research Personnel: Mark Chua, Maria Lorini
Overview:
Given the ever-present global burden of influenza virus and newly emerging pathogens such as west nile, yellow fever, and dengue virus, the study of host-virus interactions can result in discoveries that have immediate impact on human health. We focus on the study of cellular recognition and the transcriptional response to RNA virus infections in an effort to develop novel vaccine strategies. Focus areas include virus-induced cell signaling and the interplay between infection and microRNA-mediated posttranscriptional gene silencing.
Summary of Research Studies:
Recognition of viral infection. The cellular response to virus demands that the infected cell be aware of the pathogen. This is achieved by cellular proteins which identify components of virus replication that are unique to the normal biological processes of the cell. These include RNA with exposed "uncapped" 5'-ends, cytoplasmic DNA, or the formation of double stranded RNA. We are presently trying to identify additional viral associated molecular patterns and to determine how these result in downstream cellular signaling. 2. The role of the IKK-related kinases in the cellular antiviral response. Following viral recognition, the cell responds with the secretion of Type I interferon (IFN-I). This is largely coordinated by cellular kinases which mediate the activation of a number of transcription factors. These transcription factors assemble into a multisubunit complex called the enhanceosome to induce IFN-I transcription. The result of IFN-I signaling is the upregulation of a wide variety of interferon stimulated genes (ISGs) which render cells resistant to viral infection. We study two kinases critical in the induction and signaling of IFN-I through the genetic manipulation of mice and subsequent in vivo virus infections. 3. The function of miRNA in the host response to virus infection. The general cellular response to virus infection as it relates to the induction of IFNb and the antiviral response has been well defined. Virus infection induces the transcriptional induction of over 150 virus-induced genes, many of which overlap with the transcriptional profiles of IFN-I treated cells. Included in this response are the induction of greater than 30 miRNAs. Unlike typical ISG products, miRNAs are small germ-line encoded RNA species which bind to cellular and viral RNA targets to inhibit translation in a sequence-specific manner. We study the contribution of miRNA species in the host response to RNA virus infection.
Perez JT, Pham AM, Lorini MH, Chua MA, Steel J, tenOever BR. MicroRNA-mediated species-specific attenuation of influenza A virus. Nat Biotechnol 2009 Jun; 27(6): 572-576.
tenOever BR, Ng S, Chua M, McWhirter S, Garcia-Sastre A, Maniatis T. Multiple Functions of the IKK-related Kinase IKK-in Interferon Mediated Antiviral Immunity. Science 2007; 315: 1274-1278.
tenOever BR, Maniatis T. Parallel Pathways of Virus Recognition. Immunity 2006; 24: 510-512.
tenOever BR, Sharma S, Grandvaux N, Zhou GP, Lin R, Hiscott J. Triggering the Interferon Antiviral Response through an IKK-related Pathway. Science 2003; 300: 1148-1151.
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