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 and biochemical assays to identify human genes that may be able to overcome this deficiency. Our work has zeroed in on Crm1, and we are now attempting to determine why murine Crm1 is defective in terms of HIV replication.

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 high throughput identification of DNA elements that serve as transcriptional activators in various cell types, including human embryonic stem cells.

We are now funded through NIDA to use advanced genomic and genetic techniques to identify host genes associated with control of HIV in man. We are studying HIV+ elite controllers, a select subset of patients who are able to control the virus in the absence of therapy. Using a combination of molecular biology and genomic methods, we hope to pinpoint the genes causally responsible for elite control, at least in the patients who manifest a distinct in vitro phenotype. This work may inform both the HIV vaccine and eradication effort.

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.

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