Thesis (M.D.)--University of Pennsylvania, 1804. / Microform version available in the Readex Early American Imprints series.

Thesis (M.D.)--Columbia College, 1803. / Microform version available in the Readex Early American Imprints series.

Febres, quae in regionibus calidis homines invadunt, bioliosae, remittentes, vel putridae saepe appellantur ; haec autem verba morbum male definiunt, gradum enim, potius quam speciem febris, indicant.

Previous to my graduation in Edinburgh on the 1st of August 1845, I submitted to the Faculty of Medicine a Thesis on Yellow Fever. This Thesis I have since corrected and enlarged, and now venture to publish. The labour of writing it was not great, for the materials furnished to me by my father were abundant. The original copies of his manuscripts are deposited in the Army Medical Board Office in London, and may be seen by any member of the profession. The plan of my Thesis is taken in part from a manuscript copy of the Lectures on Medicine delivered by the late Dr. John Gregory in the University of Edinburgh in 1770-1771. The Appendix contains a report by my father on the Principles to be observed in providing Barracks and Hospitals for Troops in the West Indies, dated Barbados 1844; and many of these principles have since been adopted by the government.

Omissis omnibus disputationibus de nomine quod huic morbo imponi debeat, eo, quo optime cognitus est in iis regionibus, in quibus maxime grassatur, uti licebit.

"An inaugural dissertation, for the degree of Doctor of Medicine ... University of Pennsylvania, on the eighth day of June, 1803"--P. (iii). / "Errata."--P. [58]. Dedicated to Ashton Alexander, M.D., and John Parnham, M.D. Microform version available in the Readex Early American Imprints series.

"An inaugural dissertation, for the degree of Doctor of Medicine ... University of Pennsylvania, on the eighth day of June, 1803"--P. (iii). / Dedicated to Ashton Alexander, M.D., and John Parnham, M.D. "Errata."--P. [58]. Microform version available in the Readex Early American Imprints series.

Thesis (M.D.) -- University of Pennsylvania, 1804. / Microform version available in the Readex Early American Imprints series.

<p>Our ability to convert basic knowledge into robust anti-viral therapeutics requires discovery of novel host-virus interactions as well as an informed anti-viral discovery pipeline. We used a genome-scale RNAi-based screen followed by a chemical screen of FDA-approved therapeutics to identify scores of novel dengue virus (DENV) human host dependency factors (HDF) and identified more than 20 potential anti-Zika virus (ZIKV) therapeutics. </p><p>Two genes in particular, TTC35 and TMEM111, strongly inhibited DENV infection and, based on comparisons with published literature, implicated a larger protein, the ER Membrane Protein Complex (EMC), as a pan-flavivirus HDF. The EMC is a poorly characterized multiprotein complex that may function in ER-associated protein biogenesis and/or lipid metabolism. Based on our screen data, we hypothesized that the EMC is an uncharacterized HDF that functions through a common mechanism to promote replication of flaviviruses. We report that DENV, ZIKV, and yellow fever virus (YFV) infections were impressively inhibited, while West Nile Virus (WNV) infection was unchanged, in cell lines engineered to lack EMC subunit 4 (EMC4). Furthermore, targeted depletion of EMC subunits in live mosquitos significantly reduced DENV-2 propagation in vivo. In addition, the accumulation of DENV proteins shortly after infection in EMC4 knockout cells was significantly reduced, suggesting that the EMC promotes viral protein biogenesis. </p><p>We interrogated a library of FDA-approved drugs for their ability to block infection of human HuH-7 cells by a newly isolated ZIKV strain. Selected compounds were further validated for inhibition of ZIKV infection in human cervical, placental, and neural stem cell lines, as well as primary human amnion cells. Established anti-flaviviral drugs (e.g., bortezomib and mycophenolic acid) and others that had no previously known antiviral activity (e.g., daptomycin) were identified as inhibitors of ZIKV infection. Several drugs reduced ZIKV infection across multiple cell types.</p><p>We propose that the EMC may be exploited as a novel therapeutic target for multiple flaviviruses in the future. Also we identified drugs that could be tested in clinical studies of ZIKV infection and provides a resource of small molecules to study ZIKV pathogenesis.</p> / Dissertation

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