Eileen K. Bridge

Associate Professor of Microbiology

Office: 66 Pearson Hall
Phone: (513) 529-7264
Email: bridgee@MiamiOH.edu



  • MBI 131: Community Health Perspectives
  • MBI 464/564: Human Viruses
  • MBI 605: Advanced Molecular Biology
  • MBI 606: Advanced Cell Biology
  • MBI 650: Seminar in Molecular Biology
  • MBI 750H: Advanced Virology


Ph.D. in Biology, Johns Hopkins, 1990

Research Interests

Adenovirus (Ad) has been extensively studied as a model for eukaryotic molecular biology and gene expression, and it is also an important vector for gene expression and gene therapy. Ad is a DNA tumor virus, and has been an important tool for studying the development of cancer cells. Successful lytic infection by Ad requires a productive interaction with its host cell, in which the virus manipulates the cells' molecular repertoire to create an environment that is conducive to efficient viral replication. The virus promotes cell division, inhibits apoptosis, and regulates cellular DNA damage responses (DDRs) (See Fig. 1 for more details) during a productive infection. DDR activation is detrimental to efficient Ad replication. To counteract this mechanism of host interference, Ad produces regulatory proteins that inhibit DDR proteins by regulating their localization and stability. We are studying mechanisms involved in Ad activation of DDRs, and the impact of DDR activation on viral DNA replication and gene expression. These studies are expected to further our understanding of how viral genes affect host cell DNA repair activities, and may provide a basis for developing molecular tools for regulating cancer cell growth.

DNA damage response proteinsFigure 1: Ad infection has the potential to activate DNA repair proteins. Ad genomes are linear DNA molecules with attached terminal proteins. The origin of replication is located close to the ends of the viral genome. Ad early regulatory proteins from E4 inhibit the DNA damage sensor complex, which is composed of the Mre11, Rad50 and Nbs1 proteins. This prevents DDR activation and allows for a productive Ad infection cycle. Ad E4 mutants lack these critical regulatory proteins and therefore activate cellular DDR signal transduction cascades, including activation of ATM and ATR kinases, that in turn trigger signal transduction cascades that regulate apoptosis, DNA repair and cell cycle arrest. These activities interfere with E4 mutant viral DNA replication by mechanisms that are not yet understood, and result in end-to-end ligation of viral genomes when they are "repaired" to form concatemers.

Selected Publications

  • Gautam, D., Stanley, G, Owen, M, and E. Bridge. 2019. Localization of the kinase Ataxia Telangiectasia Mutated to Adenovirus E4 mutant DNA replication centers is important for its inhibitory effect on viral DNA accumulation. Virology 527:47-56.
  • Gautam, D., and E. Bridge. 2013. The kinase activity of ataxia-telangiectasia mutated interferes with adenovirus E4 mutant DNA replication. J. Virol. 87:8687-8696.
  • Prakash A, Jayaram S, and E. Bridge. 2012. Differential activation of cellular DNA damage responses by replication-defective and replication-competent adenovirus mutants. J. Virol. 86:13324-13333.
  • Mathew, S.S., and E. Bridge. 2008. Nbs1-dependent binding of Mre11 to adenovirus E4 mutant viral DNA is important for inhibiting DNA replication. Virology 374:11-22.
  • Mathew, S.S., and E. Bridge. 2007. The cellular Mre11 protein interferes with adenovirus E4 mutant DNA replication. Virology. 365:346-55
  • Jayaram, S., and E. Bridge. 2005. Genome concatenation contributes to the late gene expression defect of an adenovirus E4 mutant. Virol. 342:286-296.
  • Corbin-Lickfett, K., and E. Bridge. 2003. Adenovirus E4-34kDa requires active proteasomes to promote late gene expression. Virol. 315:234-244.