Dr. Hingley is a professor of microbiology with the Department of Bio-Medical Sciences. She teaches basic science lectures in virology, bacteriology and mycology for the DO program and the biomedical sciences program. Dr. Hingley is co-course director for the Reproductive Genitourinary and Obstetrics/Gynecologic Medicine (RGU/OB-GYN) course in the DO program. In addition, Dr. Hingley has developed case scenario exercises to supplement microbiology lecture material for the DO program.
Participate in DO courses:
Participate in Masters in Biomedical Sciences course – The Infectious Process
Dr. Hingley’s research is a collaborative study with Drs. Appelt, Little and Balin that examines a possible role for infectious agents in triggering Alzheimer's Disease. Dr. Hingley’s primary involvement is to investigate consequences of Herpes simplex virus type 1 and Chlamydia pneumoniae infection of astrocytes, either as single or dual infections. Specifically, Dr. Hingley examines the ability of one pathogen to enhance or inhibit infectivity of the second pathogen in astrocyte coinfections, as well as the effects of the two pathogens, either alone or together, on the processing of amyloid precursor protein by infected astrocytes.
Lim, C., C.J. Hammond, S.T. Hingley and B.J. Balin. 2014. Chlamydia pneumoniae infection of monocytes in vitro stimulates innate and adaptive immune responses relevant to those in Alzheimer’s disease. J. Neuroinflam. 11:217. DOI 10.1186/s12974-014-0217-0
Kenyon, L.C., Biswas K., Shindler K., Nabar M., Stout M., Hingley S.T., Grinspan J.B., Das Sarma J. 2015. Gliopathy of Demyelinating And Non-Demyelinating Strains Of Mouse Hepatitis Virus. Frontiers in Cellular Neuroscience. 9:488, ISSN:1662-5102.
Balin, B.J., Hammond, C.J., Little, C.S., Appelt, D.M., Hingley, S.T.: Evidence for
an Infectious Etiology in Alzheimer’s disease. In: Advanced Understanding of Neurodegenerative
Diseases, Raymond Chuen-Chung Chang (Ed.), ISBN: 978-953-307-529-7, Intech, Rijeka,
Das Sarma, J., L. C. Kenyon, S. T. Hingley, and K. S.Shindler . 2009. Mechanisms of primary axonal damage in a viral model of multiple sclerosis. J. Neurosci. 29:10272-10280
Shindler, K. S., L. C. Kenyon, M. Dutt, S. T. Hingley, and J. D. Sarma. 2008. Experimental optic neuritis induced by a demyelinating strain of mouse hepatitis virus. J. Virol. 82:8882-8886.
Qiu, Z., S. T. Hingley, G. Simmons, C. Yu, J. Das Sarma, P. Bates, and S. R. Weiss. 2006. Endosomal Proteolysis by Cathepsins Is Necessary for Murine Coronavirus Mouse Hepatitis Virus Type 2 Spike-Mediated Entry. J. Virol. 80:5768-5776.
Navas-Martin, S., S. Hingley, and S. R. Weiss. 2005. Murine coronavirus evolution in vivo: Functional compensation of a detrimental amino acid substitution in the receptor binding domain of the spike glycoprotein. J. Virol. 79:7629-7640.
Hingley, S. T., I. Leparc-Goffart, S. H. Seo, J. C. Tsai, and S. R. Weiss. 2002. The virulence of mouse hepatitis virus strain A59 is not dependent on efficient spike protein cleavage and cell-to-cell fusion. J Neurovirol. 8:400-10.
Das Sarma, J., L. Fu, S.T. Hingley, E. Lavi. 2001. Mouse hepatitis virus type-2 infection in mice: an experimental model system of acute meningitis and hepatitis. Exp. Mol. Pathol. 1:1-12.
Das Sarma, J., L. Fu, S.T. Hingley, M.M. Lai, E. Lavi. 2001. Sequence analysis of the S gene of recombinant MHV-2/A59 coronaviruses reveals three candidate mutations associated with demyelination and hepatitis. J Neurovirol. 5:432-436.
Navas, S., S.H. Seo, M.M.Chua, J.D. Sarma, E. Lavi, S.T. Hingley and S.R Weiss. 2001. Murine coronavirus spike protein determines the ability of the virus to replicate in the liver and cause hepatitis. J Virol. 75(5):2452-7.
Leparc-Goffart, I., S.T. Hingley, M-M. Chua, J. Phillips, E. Lavi and S.R. Weiss. 1998. Targeted recombination within the spike gene of murine coronavirus MHV-A59: Q159L is a determinant of hepatotropism. J. Virol. 72:9628-99636.
Hingley, S.T., I. Leparc-Goffart and S.R. Weiss. 1998. The spike protein of murine coronavirus MHV-A59 is not cleaved in primary glial cells and primary hepatocytes. J. Virol. 72:1606-1609.
Christine Hammond, Jonathan M Anzmann, Abhi P Jain, Susan T Hingley, Brian J Balin.
Cellular modeling of inflammation relevant to Alzheimer's disease: Molecular and cytokine
analysis of host responses following chlamydial infection of human thp-1 monocytes.
Alzheimer's and Dementia Vol. 12 Iss. 7 (2017) p. P628
Denah M. Appelt, Christopher A. Cappellini, Ahmad B. Cader, Keith G. Williams, Juliana D. Zoga, Susan T. Hingley, Marcus G. Bell, Brian J. Balin. 2013. Changes in calcium-related gene expression consistent with Alzheimer’s disease are initiated by infection of neuronal cells with Chlamydia pneumoniae. Presented at the International Conference on Alzheimer’s Disease
Christopher A. Cappellini, Ahmad B. Cader, Keith G. Williams, Juliana D. Zoga, Susan T. Hingley, Brian J. Balin, Denah M. Appelt, Marcus G. Bell. 2013. Chlamydia pneumoniae infection of neuronal cells induces changes in calcium-associated gene expression consistent with Alzheimer’s disease. Presented at the Chlamydia Basic Science Research Meeting
Denah Appelt, Ian Kohler, Annette Slutter, Juliana Zoga, Susan T. Hingley, Brian Balin. 2012. Autophagy and apoptotic genes implicated in Alzheimer’s disease are modulated following infection of neuronal cells with Chlamydia pneumoniae. Presented at the International Conference on Alzheimer’s Disease
Ian Kohler, Annette Slutter, Juliana Zoga, Susan T Hingley, Brain Balin, Denah Appelt. 2012. Genetic dysfunction related to Alzheimer’s disease is found in neuronal cells after short-term and long-term Chlamydia pneumoniae infection. Presented at the Society for Neuroscience
Marcus Bell, Keith Williams, Juliana Zoga, Susan Hingley, Brian Balin, Denah Appelt. 2012. Alzheimer’s disease-like changes in calcium associated gene expression and protein regulation following C. pneumoniae infection of neuronal cells and monocytes. Presented at the Society for Neuroscience
Morgan M. Devins, Fiora D. Zoga, Brian J.Balin, Denah M. Appelt, Susan T. Hingley. 2011 Infection of neuronal cells by Chlamydia pneumoniae and Herpes simplex virus type 1 alters expression of genes associated with Alzheimer’s disease. Presented at the Society for Neuroscience
K. Cade, J. Romer, S. Hingley, 2011. Entry mechanisms of mouse hepatitis virus is more dependent on clathrin- than caveolin-mediated pathways. Presented at the XIIth International Nidovirus Symposium
K. Kralik, D. Tabello, J. Das Sarma, S. Hingley. 2008. Entry of murine coronavirus MHV-A59 involves both clathrin-dependent and caveolin-dependent pathways. Presented at the XIth International Nidovirus Symposium
K. Kralik, L. Triplett, J. Das Sarma, S. Hingley. 2007. The entry pathway used by murine coronavirus MHV-A59 is dependent on host cell type. Presented at American Society for Virology 26th Annual Meeting
L. R. Triplett, K. S. Kralik, B. J. Balin, S. T. Hingley, D. M. Appelt. 2007. Analysis of Aβ 1-42 amyloid in neuronal cells infected with Herpes Simplex Virus 1 and Chlamydophila (Chlamydia) pneumoniae. Presented at Federation for American Societies for Experimental Biology Annual Meeting
2007-2008 – CCDA Pilot Research Project: Development of a real-time PCR assay for the investigation of viral entry mechanisms
2008-2011 – Health Research Formula Fund: Entry Mechanisms of Mouse Hepatitis Virus, an animal model for multiple sclerosis
2010-2011 – CCDA Pilot Research Project: Changes in expression of genes associated with Alzheimer’s disease and β-amyloid processing due to infection of neuronal cells by Chlamydia pneumoniae and/or herpes simplex virus type 1