Thomas Gallagher, PhD
Ph.D. University of Wisconsin
Major Research Interests: Molecular Mechanisms of Virus Assembly and Entry.
Our primary research interests are in virology. We specifically focus our attention on human pathogenic coronaviruses, such as the Severe Acute Respiratory Syndrome (SARS) and Middle East Respiratory Syndrome (MERS) coronaviruses. These coronaviruses transmit into humans from infected animals, causing a severe pneumonia that can be fatal in elderly or immune-compromised patients. Coronavirus’ potential to cause respiratory disease is related to its capacity to enter and infect lung cells. We use lung-derived cells to dissect the virus entry process, and we relate these cell entry processes with viral pathogenesis, through collaborations with laboratories developing small animal models of human coronavirus-induced respiratory disease. Together these research activities identify determinants of human pneumovirulence in zoonotic pathogens.
We also focus on extracellular vesicles. These are enveloped virus-like particles that can transfer their contents between cells, thereby generating biological responses ranging from wound healing to tumor progression. We compare and contrast enveloped virus and extracellular vesicle – mediated transfer of cytoplasmic contents between cells. We aim to identify the components that allow extracellular vesicles to transfer cytoplasmic cargoes between cells.
Our research programs utilize the tools of modern molecular and cellular biology to explain how viruses and vesicles disseminate through organisms and thereby cause disease. Our programs are dedicated to the education of Loyola postdoctoral fellows, PhD and MS students, summer MD students, undergraduate interns, and research assistants.
Park, J.-E. and Gallagher, T. (2017) Lipidation increases antiviral activities of coronavirus fusion-inhibiting peptides. Virology 511: 9-18. http://dx.doi.org/10.1016/j.virol.2017.07.033
Earnest, J.T., Hantak, M.P., Li, K., McCray, P.B., Perlman, S., and Gallagher, T. (2017) The tetraspanin CD9 facilitates MERS coronavirus entry by scaffolding host cell receptors and proteases. PLOS Pathogens 13(7):e1006546. https://doi.org/10.1371/journal.ppat.1006546.
Li, K., Wohford-Lenane, C.L., Channapanavar, R., Park, J.-E., Earnest, J.T., Bair, T.B., Bates, A.M., Brogden, K.A., Flaherty, H.A., Gallagher, T., Meyerholz, D.K., Perlman, S., and McCray, P.B. (2017) Mouse-adapted MERS coronavirus causes lethal lung disease in human DPP4 knockin mice. Proc. Natl. Acad. Sci. USA doi/10.1073/pnas.1619109114
Phillips, J.M., Gallagher, T., and Weiss, S.R. (2017) Neurovirulent murine coronavirus JHM.SD uses cellular zinc metalloproteases for virus entry and cell-cell fusion. J. Virol. PMID: 28148786 DOI: 10.1128/JVI.01564-16
Park, J.-E., Li, K., Barlan, A., Fehr, A.R., Perlman, S., McCray, P.B., and Gallagher, T. (2016) Proteolytic processing of Middle East respiratory syndrome coronavirus spikes expands virus tropism. Proc. Natl. Acad. Sci. USA 113:12262-12267 doi/10.1073/pnas.1608147113
Earnest, J.T., Hantak, M.A., Park, J.-E., and Gallagher, T. (2015) Coronavirus and influenza virus proteolytic priming takes place in tetraspanin-enriched membrane microdomains. J Virol, 89(11): p. 6093-6104. PMCID: PMC4442435
Zhao, J., Li, K., Wohlford-Lenane, C., Agnihothram, S., Fett, C., Zhao, J., Gale, M., Baric, R., Enjuanes, L., Gallagher, T., McCray, P., Perlman, S. (2014) Rapid generation of a mouse model for middle east respiratory syndrome. Proc. Natl. Acad. Sci. USA 4970-4975. PMCID: PMC3977243
Barlan, A., Zhao, J., Sarkar, M., Li, K., McCray, P., Perlman, S., and Gallagher, T. (2014) Receptor variation and susceptibility to middle east respiratory syndrome coronavirus infection. J. Virol. 88: 4953-4961. PMCID: PMC3993797
A complete bibliography can be found online.