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Thomas Gallagher, PhD

Microbiology / Immunology

Bio

  • Professor

Ongoing Research

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.

Education

  • Ph.D. University of Wisconsin

Research Interests

  • Molecular Mechanisms of Virus Assembly and Entry

Publications/Research Listings

  • 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.