Glenn F. Rall, PhD

Glenn Rall, PhD


Chief Academic Officer

Brain Cancer TRDG Member

Research Program

Evidence of measles virus antigens in dendritic spines
Evidence of measles virus antigens in dendritic spines. Primary embryonic hippocampal neurons were plated and infected with measles virus (MOI=3); samples were collected 48 hours post-infection and labeled for cell nuclei (blue; Hoescht stain), dendrites (green) and measles virus antigens (red). Magnification 400X; imaging by Imaris software
Rall lab staff, 2015


Education and Training

Educational Background

  • Postdoctoral, Viral Immunology, The Scripps Research Institute, La Jolla, CA, 1990-95
  • PhD, Microbiology and Immunology, Vanderbilt University, Nashville, TN, 1990
  • BS, with Honors, Biology, Lafayette College, Easton, PA, 1985


  • American Society of Microbiology
  • American Association of Immunology
  • American Society of Virology

Honors & Awards

  • The Sidney Pestka Lecturer, American Society for Microbiology, 2014
  • Dozor Lecturer, Ben-Gurion University, 2007
  • Autism Speaks Scientific Advisory Member of the Year, 2007
  • F.W. Kirby Scholar in Neurodegenerative Disease, 1998-present
Research Profile

Research Program

Research Interests

Viral infection, immunity and disease in the brain

  • Elucidating how neurotropic viruses spread to, and across, synaptic junctions
  • Defining principles that govern unique aspects of the host immune response within the brain
  • Developing mouse models to study immunity to multiple pathogenic encounters
  • Evaluating long-term neuropathological consequences of viral infections

Lab Overview

Our laboratory studies viral infections of the brain and the immune responses to those infections, with the goal of defining how viruses contribute to disease in humans, including cancer. Over the past decade, we have developed mouse models that have enabled mechanistic insights into viral replication and spread within neurons, and the roles played by soluble immune mediators, such as chemokines and cytokines, in viral clearance.

A primary objective of our work is to understand how the immune response contributes to viral clearance from the central nervous system without inducing brain damage, such as encephalitis or edema. Using a transgenic mouse model that restricts measles virus infection to CNS neurons, we have shown that both type I and type II interferons play a crucial role in clearance. Interferons, especially the type I interferons, alpha and beta, are used clinically to dampen virus infections that are associated with human cancer, such as hepatitis C. However, we do not fully understand how these immune molecules function in vivo; thus, a manipulable animal model system will be essential for understanding their mode of action, and how they may cause CNS pathology. Moreover, immunotherapy has particular appeal for the resolution of brain tumors that are otherwise not approachable with existing surgical, radiological or chemical strategies. However, immunotherapeutic side effects, such as edema, pose a particular concern in the brain. Therefore, clarifying how a CNS immune response can occur without induction of immunopathology—as in our model system—is directly relevant to the development of immune-mediated approaches to resolve CNS tumors.

Lab Staff

Christine Matullo, PhD

Postdoctoral Associate

Room: R493

Katelyn Miller

Graduate Student

Room: R493

Andreas Solomos

Graduate Student

Room: R493

Additional Staff

Virginia Pearson, Visiting Scientist

Yianna Yiantsos, Undergraduate Intern


Selected Publications

O’Donnell, L.A., K. M. Henkins, A. Kulkarni, C. M. Matullo, S. Balachandran, A. K. Pattisapu, G. F. Rall.  Interferon gamma induces protective, non-canonical signaling pathways in primary neurons. J. Neurochem., 135: 309-322, 2015. PMID: 26190522 PubMed

Miller, K.D., Holmgren, A.M., S.E. Cavanaugh, G.F. Rall.  Bone marrow stromal antigen-2 (Bst2)/tetherin is induced by type I interferon and viral infection, but is dispensable for protection against neurotropic viral challenge.  J. Virology, 89: 11011-11018, 2015. PMID: 26311886 PubMed

Cavanaugh, S.E., A.M. Holmgren, G.F. Rall.  Homeostatic interferon expression in neurons is sufficient for early control of viral infection.  J. Neuroimmunol, 279: 11-19, 2015. PMC4325274 PubMed

Thapa, R.J., S. Nogusa, P. Chen, J.L. Maki, A. Lerro, M. Andrake, G.F. Rall, A. Degterev, S. Balachandran.  Interferon-induced RIP1/RIP3-dependent necrosis requires PKR and is licensed by FADD and caspases.  Proc. Natl. Acad. Sci., 110: E3109-118, 2013.  PMC3746924 PubMed

O'Donnell, L.A., S. Conway, R.W. Rose, E. Nicolas, M. Slifker, S. Balachandran, G.F. Rall.  STAT-1 independent control of a neurotropic measles virus challenge in primary neurons and infected mice.  J. Immunol., 188 (4): 1915-1923, 2012. PMCID: PMC3273675 PubMed

Gomme, E.A., C. Wirblich, S. Addya, G.F. Rall, M.J. Schnell.  Immune clearance of attenuated rabies virus results in neuronal survival with altered gene expression.  PLoS Pathogens, 8 (10):  e1002971, 2012. PMCID: PMC3469654 PubMed

Matullo, C.M., K.J. O’Regan, M. Curtis, G.F. Rall. CNS Recruitment of CD8+ T Lymphocytes specific for a peripheral virus infection triggers neuropathogenesis during polymicrobial challenge. PLoS Pathogens, 7 (12): e1002462, 2011. PMCID: PMC3245314 PubMed

Matullo, C.M., K.J. O'Regan, M. Curtis, H. Hensley, G.F. Rall.  Lymphocytic choriomeningitis virus-induced mortality in mice is triggered by edema and brain herniation.  J. Virol., 84: 312-320, 2010. PMCID: PMC2798401 PubMed

Rose, R.W., A. Vorobyeva, J.D. Skipworth, E. Nicolas, G.F. Rall.  Altered levels of STAT1 and STAT3 influence the neuronal response to interferon gamma.  J. Neuroimmunol, 192: 145-156, 2007. PMCID: PMC2180831 PubMed

Makhortova, N., P. Askovich, C. E. Patterson, L. A. Gechman, N. P. Gerard, G. F. Rall. Neurokinin-1 enables measles virus trans-synaptic spread in neurons.  Virology, 362: 235-244, 2007. PMCID: PMC1945128 PubMed

Additional Publications


This Fox Chase professor participates in the Undergraduate Summer Research Fellowship
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