Jay R. Radke, PhD


Faculty Positions

  • Associate Research Scientist
  • Idaho Veterans Research & Education Foundation
  • Boise VA Medical Center
  • Boise State University Department of Biological Sciences – Affiliated Faculty
  • Boise State University Biomolecular Sciences Graduate Program – Affiliated Faculty
  • Idaho State University Department of Biomedical and Pharmaceutical Sciences – Allied Faculty
Back to Researchers


  • B.S. Biology/Microbiology – University of Wisconsin Milwaukee
  • M.S. Microbiology and Molecular Genetics – Medical College of Wisconsin
  • Ph.D. Microbiology and Immunology – University of Illinois at Chicago


Research in the Radke laboratory is focused on understanding both viral and host factors that alter innate immune responses to severe respiratory viral infection leading to acute respiratory distress syndrome (ARDS) in order to begin to design novel therapeutic treats to prevent/treat virus induced ARDS. Our studies use an emergent strain of human Adenovirus 14 (Ad14p1) which is predominant strain of Ad14 circulating around the world and is responsible for multiple outbreaks in populations annually. These infections are more severe than standard Adenovirus infections in otherwise healthy individuals and can result in severe, acute lung injury and, in some cases, ARDS which has resulted in fatalities. Syrian hamsters are permissive for human adenoviruses. We have shown that infection of Syrian hamsters with Ad14p1 infection induces a patchy bronchopneumonia and increased inflammatory cytokine expression in the lungs that is not seen following infection with prototype Ad14 strain (de Wit). We have described a novel, immunorepressive activity of Ad infected dying cells (termed Ad CPE corpses) that modulate the Ad-induced, innate immune response. Ad CPE corpse repression of macrophage-mediated inflammatory responses requires expression of the Ad protein, E1B 19/20K. Ad CPE corpses resulting from infection with Ad that lack E1B 19/20K, fail to repress Ad-induced macrophage pro-inflammatory responses and, in contrast, can induce increases in such responses. Ad14p1 infected cells express only ~20% of the E1B 19/20K protein compared to Ad14. Despite being 99.9% genetically identical there are other ways Ad14p1 differs from Ad14 besides E1B 19/20K expression. We have identified cellular miRNAs that are more abundantly expressed in Ad14 CPE corpses than in Ad14p1 CPE corpses and have been shown to play a role in down regulating pro-inflammatory signal transduction pathways and cytokine expression. Adenovirus also encode RNA molecules which can be processed by Dicer into virally encoded miRNAs. In recent studies we have shown that there is differential expression of these Ad encoded miRNAs between Ad14 and Ad14p1 infected cells. There are also scattered mutations in Ad14p1 genes that result in amino acid changes in expressed viral proteins that may alter the innate immune response during infection. Our current research is focused on how these changes in host/viral miRNA expression as well as changes in viral protein expression/function contributes to the pathogenesis of Ad14p1. We are beginning studies to understand how host factors such as diabetes result in increased morbidity/mortality from respiratory viral infections from emergent strains of Adenovirus and influenza.

Current Projects

  • Understanding the roles of macrophages and cellular miRNA during respiratory virus-induced acute lung injury in diabetic and non-diabetic Syrian hamsters
  • The role of viral miRNAs in differential inflammatory responses of macrophages to Ad14 and Ad14p1 CPE corpses.
  • Defining the Ad14 and Ad14p1 viral transcriptomes in infected cells.
  • Unlocking the effects of Ad14 and Ad14p1 infection on the host signal transduction pathways that lead to inflammatory cytokine expression.
  • Characterizing the functions of Ad14 and Ad14p1 E3 proteins during infection.
  • Increasing the usefulness of the Syrian hamster as a model organism to study infectious diseases by improving the Syrian hamster genome annotation for use in single cell RNA-seq studies and development of antibodies to identify Syrian hamster immune cells by flow cytometry.

Other Research Interests and Expertise

  • Effects of virus infection and viral proteins of cell death pathways using flow cytometry
  • Expression of Adenovirus E1A protein to sensitize tumor cells to chemotherapeutic agents and innate immune effector cells such as activate macrophages and NK cells
  • Tumor induction studies in nude mice
  • Development of recombinant Adenoviruses for therapeutic uses such as oncolytic/chemo-sensitization

Current Funding

  • Interrogating cell signaling pathways during Ad14p1 lung pathogenesis. Idaho INBRE Developmental Research Project
  • The role of miR-181a-5p in Adenovirus 14p1 induced acute lung injury. NIH R21 RAI162464A
  • The role of macrophages and miRNA in regulating lung macrophage polarization and lung pathogenesis during respiratory virus-induced acute lung injury in normal and diabetic Syrian hamsters. VA Merit Award – Pending Notice of Award