Dr. Shelton Bradrick


Laboratory Web Page

Affiliation: Department of Biochemistry & Molecular Biology
Tel: (409) 772-2749
Route: 1055
5.138C MRB

Shelton S. Bradrick, Ph.D.

Assistant Professor

I am interested in pathogenic human RNA viruses and the molecular biology of host response to infection. There are currently two areas of research focus:

  1. We study regulation of cellular interferon responses to RNA virus infection. Of particular interest are a class of interferons that provide first line defense against viruses that infect epithelial tissues. These cytokines, termed interferon-lambdas (IFNLs), have been strongly implicated in control of Hepatitis C virus (HCV), a liver-tropic virus associated with significant global mortality. We study mechanisms by which IFNL genes are regulated post-transcriptionally and how genetic polymorphisms shape the response to HCV infection. Using a combination of proteomic, cell-based and cell-free assays, we aim to dissect IFNL gene regulation with the expectation that our investigations will reveal new factors and mechanisms that impact cytoplasmic gene expression in general.
  2. In collaboration with my co-Principal Investigator in the Department of Biochemistry and Molecular Biology, Dr. Mariano Garcia-Blanco, we are pursuing projects involving molecular host-pathogen interactions for several arthropod-borne flaviviruses, including Dengue virus (DENV) and the Yellow Fever virus (YFV). Like HCV, replication of these plus-strand RNA viruses is dependent on, or restricted by, host-encoded RNA and protein factors. We are particularly interested in the identification and characterization of RNA-protein interactions that regulate viral replication and host gene expression in the cytoplasm. Specific projects include: (i) elucidating the role of particular ribosomal proteins in the flavivirus life-cycle, (ii) RNA affinity chromatography to isolate DENV ribonucleoprotein complexes from infected cells, and (iii) characterizing roles for the endoplasmic reticulum and associated resident proteins in early phases of the flavivirus life-cycle.