Ruth Everett
Duke University
7 Papers
258 Citations
Ruth Everett is an academic researcher from Duke University. The author has contributed to research in topics: Innate immune system & Immune system. The author has an hindex of 6, co-authored 7 publications. Previous affiliations of Ruth Everett include University of Arkansas for Medical Sciences & University of California, Los Angeles.
Chat about Author
Papers
Adenovirus Infection Triggers a Rapid, MyD88-Regulated Transcriptome Response Critical to Acute-Phase and Adaptive Immune Responses In Vivo
Zachary C. Hartman,Anne Kiang,Ruth Everett,Delila Serra,Xiao Y. Yang,Timothy M. Clay,Andrea Amalfitano +6 more
TL;DR: Bioinformatics-based transcriptome analysis revealed a complex innate response to Ad infection, with induction of proinflammatory responses (and suppression of metabolism and mitochondrial genes) akin to those observed when mice are challenged with lipopolysaccharide.
146
Liver Toxicities Typically Induced by First-Generation Adenoviral Vectors Can Be Reduced by Use of E1, E2b-Deleted Adenoviral Vectors
TL;DR: Improvements in vector safety rival those noted with other, more significantly modified Ad vectors described to date and demonstrate a marked reduction in maximal liver toxicities and pathologies with the use of the [E1(-), E2b(-)] modified vector in all strains of mice tested.
78
Adenovirus Vectors with the 100K Gene Deleted and Their Potential for Multiple Gene Therapy Applications
TL;DR: The unique properties of [100K−]Ad vectors suggest that they may have utility in a variety of gene therapy applications, based upon its ability to increase the copy number of the transgene encoded by the vector while decreasing the side effects associated with Ad late gene expression.
50
Strain-specific rate of shutdown of CMV enhancer activity in murine liver confirmed by use of persistent [E1(-), E2b(-)] adenoviral vectors.
TL;DR: This study confirmed that [E1(-), E2b(-)]Ad vector genomes could persist equally well in C57Bl/6 or Balb/c mouse hepatocytes, and observed a strain-dependent variability in the duration of CMV enhancer/promoter-driven transgene expression in the liver.
34