Susan T. Hingley, PhD
Dr. Susan Hingley is a Professor with the Department of Pathology, Microbiology, Immunology and Forensic Medicine at PCOM. She teaches basic science lectures in Virology, Microbiology and Mycology for the DO program, and is Course Director of The Infectious Process course for the Masters in Biomedical Sciences Program. Dr. Hingley is a member of the American Society of Virology, American Society of Microbiology and the International Society for Neurovirology.
Dr. Hingley received her PhD in Microbiology from Temple University School of Medicine in 1987. She did a postdoctoral fellowship in Microbiology at Hahnemann University School of Medicine, and one in Virology at the University of Pennsylvania School of Medicine. Dr. Hingley came to PCOM in 1994.
Research
Dr. Hingley's current research involves investigating, on a molecular level, the pathogenesis of mouse hepatitis virus (MHV). Neurovirulent strains of MHV are studied as animal models for demyelinating diseases such as Multiple Sclerosis. Her work focuses on the role of the viral fusion glycoprotein in pathogenesis; current research is directed at understanding entry mechanisms of MHV mediated by the fusion glycoprotein. Dr. Hingley is also involved in a collaborative study with Dr. Denah Appelt that examines a possible role for infectious agents in triggering Alzheimer's Disease. Drs. Hingley and Appelt are investigating amyloid production and processing in cells infected with Chlamydia pneumonia and/or Herpes simplex virus.
Email: susanh@pcom.edu
Awards
CCDA Pilot Research Project; 2007
Development of a real-time PCR assay for the investigation of viral entry mechanisms
Publications
Endosomal Proteolysis by Cathepsins Is Necessary for Murine Coronavirus Mouse Hepatitis Virus Type 2 Spike-Mediated Entry. Qiu, Z., S. T. Hingley, G. Simmons, C. Yu, J. Das Sarma, P. Bates, and S. R. Weiss, 2006. J. Virol. 80:5768-5776.
Murine coronavirus evolution in vivo: Functional compensation of a detrimental amino acid substitution in the receptor binding domain of the spike glycoprotein. Navas-Martin, S., S.T. Hingley, and S. R. Weiss, 2005. J. Virol.
79:7629-7640.
The virulence of mouse hepatitis virus strain A59 is not dependent on efficient spike protein cleavage and cell-to-cell fusion. Hingley, S. T., I. Leparc-Goffart, S. H. Seo, J. C. Tsai, and S. R. Weiss. 2002. J. Neurovirol. 8:400-410.
Sequence analysis of the S gene of recombinant MHV-2/A59 coronaviruses reveals three candidate mutations associated with demyelination and hepatitis. Das Sarma, J., L. Fu, S. T. Hingley, M. M. Lai, and E. Lavi. 2001. J. Neurovirol. 7:432-436.
Role of the spike protein in murine coronavirus induced hepatitis: an in vivo study using targeted RNA recombination. Navas, S., S. H. Seo, M. M. Chua, J. Das Sarma, S. T. Hingley, E. Lavi, and S. R. Weiss. 2001. Adv. Exp. Med. Biol. 494:139-144.
Murine coronavirus spike protein determines the ability of the virus to replicate in the liver and cause hepatitis. Navas, S., S. H. Seo, M. M. Chua, J. D. Sarma, E. Lavi, S. T. Hingley, and S. R. Weiss. 2001. J. Virol. 75:2452-2457.
Mouse hepatitis virus type-2 infection in mice: an experimental model system of acute meningitis and hepatitis. Sarma, J. D., L. Fu, S. T. Hingley, and E. Lavi. 2001. Exp. Mol. Pathol. 71:1-12.
The mouse hepatitis virus A59 spike protein is not cleaved in primary hepatocyte and glial cell cultures. Hingley, S. T., I. Leparc-Goffart, and S. R. Weiss. 1998. Adv. Exp. Med. Biol. 440:529-535.
The spike protein of murine coronavirus mouse hepatitis virus strain A59 is not cleaved in primary glial cells and primary hepatocytes. Hingley, S. T., I. Leparc-Goffart, and S. R. Weiss. 1998. J. Virol. 72:1606-1609.
Targeted recombination within the spike gene of murine coronavirus mouse hepatitis virus-A59: Q159 is a determinant of hepatotropism. Leparc-Goffart, I., S. T. Hingley, M. M. Chua, J. Phillips, E. Lavi, and S. R. Weiss. 1998. J. Virol. 72:9628-9636.