Katherine R Spindler, PhD

Dr. Spindler worked on two viruses in graduate school: the bacteriophage ΦX174 and vesicular stomatitis virus (VSV). For her dissertation with John Holland, she investigated the virus evolution during persistent infection by VSV. Dr. Spindler moved to UCLA for her postdoctoral work on adenoviruses with Arnie Berk, where she used molecular biology tools to characterize viral gene expression and viral replication.

Since the human adenoviruses are species-specific, in order to study viral pathogenesis she began studies with mouse adenovirus (MAV-1) in mice. Dr. Spindler’s first faculty position was in the Department of Genetics at the University of Georgia. Eighty-three people worked on MAV-1 in the Spindler lab in Athens. In 2002 Kathy moved to a position as Professor in the Department of Microbiology & Immunology at the University of Michigan. More than 100 people have worked in the Spindler lab in Ann Arbor.

Dr. Spindler’s research encompassed virology, pathogenesis, molecular biology, genetics, immunology and even some biochemistry. In addition to being a member of the U-M M&I Department, she was a member of the Cellular and Molecular Biology Training Program and the Molecular Mechanisms of Microbial Pathogenesis Training Program. She was Secretary-Treasurer of the American Society for Virology for seven years and has been a member of the TWiV podcast team ("This Week in Virology") since 2012.

Dr. Spindler had a longstanding interest in determining viral and host determinants of pathogenesis. Initial research included characterizing the molecular genetics of mouse adenovirus type 1 (MAV-1). Subsequent projects included identifying host genetics of mouse susceptibility to MAV-1, mechanisms of MAV-1 disruption of the blood-brain barrier, and innate immune responses to MAV-1 infection. Her recent research addressed how MAV-1 interacts with host eIF2-alpha kinases and successfully replicates in the face of these host antiviral responses. A collection of MAV-1 mutant viruses and reagents was combined with existing mouse mutants in eIF2-alpha kinases to determine their importance to the outcome of viral infections.