Richard Sutton MD/PhD
Associate Professor of Medicine (Infectious Diseases) and of Microbial Pathogenesis
Research Interests
HIV replication and the development of small animal models of HIV; HIV vectors; HIV replication and gene transfer into non-dividing cells
Research Summary
Our laboratory is focused on the study of human immunodeficiency virus type I (HIV) replication and the development of small animal models of HIV. For example, mice are not susceptible to HIV due a profound block in HIV assembly and release from cells. We are exploring the nature of this block and are conducting genetic screens to identify human genes that may be able to overcome this deficiency.
This has led to an innovative method of making nested intrachromosomal deletions, which could be used to identify previously unknown tumor suppressors and genes involved in developmental defects. We also utilize replication-defective HIV as a vector to transduce non-dividing cells for gene therapeutic purposes and are developing novel methods of vector production. These vectors are used to investigate other viruses (for example, cellular binding and entry requirements of Ebola and Western Equine Encephalitis) and to explore fundamental questions in molecular biology, such as the fidelity of RNA polymerase II.
Selected Publications
- Wang, P. et al. UBXN1 Interferes with Rig-I-like Receptor-Mediated Antiviral Immune Response by Targeting MAVS. Cell Reports, in press.
- Elinav, H. et al. Human CRM1 augments production of infectious human and feline immunodeficiency viruses from murine cells. J. Virology 86: 12053-68, 2012.
- Engin, F. et al. (2009) Notch signaling contributes to the pathogenesis of human osteosarcomas. Human Mol. Genetics 18: 1464-70.
- Poluri, A, & Sutton, RE. (2008) Functional pseudotyping of western equine encephalitis virus glycoprotein with human immunodeficiency virus type 1 vectors, Journal of Virology 82: 12580-4.
- Poluri, A & Sutton, RE. (2008). Titers of HIV-based vectors encoding shRNAs are reduced by a dicer-dependent mechanism. Mol Ther. 16: 378-386.



