Ricardo Rajsbaum, PhD
Microbiology & Immunology
Phone: (409) 772-4917
Education: PhD | 2009 | MRC National Institute for Medical Research, London, England
MSc | 1999 | Weizmann Institute of Science, Rehovot, Israel
BSc | 1996 | Universidad Nacional Autonoma de Mexico, Mexico
Overview: Innate immunity to virus infection. Pattern recognition receptor signaling, ubiquitin and E3- ubiquitin ligases in regulation of virus replication. Antagonism of innate immune response by viruses.
Work in the Rajsbaum laboratory focuses on the study of host-pathogen interactions and innate immune responses to viruses. Innate and cell-intrinsic immune responses are essential to protect host cells against pathogens. Members of the tripartite motif (TRIM) family of E3-ubiquitin ligases are involved in antiviral immunity by directly inhibiting viral replication or by sensing and transmitting signals to induce antiviral cytokines. However, to establish productive infection, viruses have developed sophisticated mechanisms to counteract host immune responses, including targeting TRIM proteins. Our lab is interested in elucidating the mechanisms by which TRIM proteins and other signaling molecules regulate antiviral functions and how viruses (Influenza, dengue, Zika, West Nile, Ebola, Nipah and other viruses) evade these immune responses. We and others have shown that members of the TRIM family (TRIM5, TRIM6, TRIM25) catalyze the synthesis of unanchored polyubiquitin chains that activate antiviral signaling pathways. In addition, new evidence indicates that TRIMs and ubiquitination of viral proteins can have both antiviral and proviral functions depending on the host environment. Our lab aims to dissect these molecular mechanisms that regulate virus replication using in vitro biochemical methods, primary immune cells, and in vivo animal models. We also hope to identify new components of innate immune signaling pathways and viral factors that could be targeted for therapeutic intervention.