People

Ethan Will Taylor

Ethan WIll Taylor
Title: Professor
Field: Biomedicinal Chemistry
Room: 403A Sullivan Science Building, JSNN 106M
Phone: 336.285.2890
Email: ewtaylor@uncg.edu
Research Website: https://chem.uncg.edu/person/e-will-taylor/

Education

B.Sc. (Chemistry), University of Winnipeg , 1981
Ph.D. (Pharmacology), University of Arizona , 1985
NIH Postdoc (Medicinal Chemistry), University of Arizona, 1986-1987


Research

Research interests and activities of the Taylor lab encompass areas ranging from structural bioinformatics, molecular modeling and drug design, to applied molecular biotechnology, nanotechnology and virology, with a special focus on the biochemistry of the dietary trace element selenium.

Molecular modeling, bioinformatics, virus gene discovery and identification. Our research often begins with theoretical genomic analysis, using various bioinformatics tools, to develop hypotheses about biological structure and mechanisms, which are then validated in the “wet lab” by molecular biological methods. This approach is applied to various problems of biomedical interest. A key accomplishment is our demonstration that the genomic complexity of some viruses is greater than previously thought. In the case of HIV-1 we have demonstrated the existence of several novel viral proteins encoded in “hidden” genes, and shown that they function as previously predicted by theory. These findings have implications for the role of dietary antioxidants, and the trace mineral selenium in particular, in modulating viral pathogenesis.

The SARS coronaviruses as a paradigm for the perturbation of host selenobiology by RNA viruses. In a study of COVID-19 patients in China, Dr. Taylor and an international team of scientists were the first to demonstrate a significant, positive association between regional selenium status and the outcome of SARS-CoV-2 infection (article #10 listed below). These findings are similar to widely reported results about COVID-19 severity being affected by host vitamin D3 status, which may act synergistically with selenium, because it is well established that vitamin D3 increases the expression of several selenium-containing proteins and other antioxidant and anti-inflammatory genes. Significantly, we have shown that, by antisense and/or proteolysis, SARS-CoV-2 may be targeting genes that are upregulated by Se and/or vitamin D3 (e.g. thioredoxin reductase 1, glutathione peroxidase 1, and enzymes involved in glutathione synthesis), resulting in virus-mediated knockdown at both the mRNA and protein levels (articles #9, 11 and 12 listed below). Most of these genes are involved in DNA synthesis, so their knockdown by SARS-CoV-2, an RNA virus, may serve to increase the pool of ribonucleotides, to increase the production of viral RNA for incorporation into progeny viruses. Disruption of host antioxidant defenses with increased oxidative stress, inflammation and cell death can be seen as “collateral damage” from these viral mechanisms. Deficiencies of selenium, vitamin D3 or glutathione would exacerbate the resulting pathogenic effects.

Representative Publications

(from a total of over 80 research articles and book chapters)

  1. Zhao, L., Cox, A.G., Ruzicka, J.A., Bhat, A.A., Zhang, W. and Taylor E.W. (2000): Molecular modeling and in vitroactivity of an HIV-1 encoded glutathione peroxidase.  Proc. Natl. Acad. Sci. USA 97: 6356-6361.
  2. Olubajo, B. and Taylor, E.W. (2005) A -1 frameshift in the HIV-1 env gene is enhanced by arginine deficiency via a hungry codon mechanism. Mutat. Res. 579: 125-132.
  3. Chandrasekaran, V. and Taylor, E.W. (2007) Molecular modeling of the oxidized form of Nuclear Factor-κB suggests a mechanism for redox regulation of DNA binding and transcriptional activation. J. Mol. Graph. Model. 26: 861-7.
  4. E. Kleinman, K. Yamada, A. Takeda, V. Chandrasekaran, M. Nozaki, J.Z. Baffi, R.J.C. Albuquerque, S. Yamasaki, M. Itaya, Y. Pan, B. Appukuttan, D. Gibbs, Z. Yang, K. Karikó, B.K. Ambati, T.A. Wilgus, L.A. DiPietro, E. Sakurai, K. Zhang, J.R. Smith, E.W. Taylor, J. Ambati (2008) Sequence- and target-independent suppression of angiogenesis by siRNA via TLR3. Nature, 452: 591-597.
  5. Taylor, E.W. (2009) The oxidative stress-induced niacin sink (OSINS) model for HIV pathogenesis. Toxicology 278: 124-130.
  6. Carlsen, A., Zahid, O., Ruzicka, J., Taylor, E.W., and Hall, A.R. (2014) Interpreting the Conductance Blockades of DNA Translocations Through Solid-State Nanopores.  ACS Nano. 8(5):4754-60.
  7. Taylor, E.W., Ruzicka, J.A., Premadasa, L. and Zhao, L. (2016) Cellular selenoprotein mRNA tethering via antisense interactions with Ebola and HIV-1 mRNAs may impact host selenium biochemistry.  Curr. Top. Med. Chem., 16, 1530-1535.
  8. Zahid, O., Wang, F., Ruzicka, J.A., Taylor, E.W., and Hall, A.R. (2016)  Sequence-Specific Recognition of MicroRNAs and Other Short Nucleic Acids with Solid-State Nanopores. Nano Lett. 16: 2033–2039.
  9. Taylor, E. W. (2020) RNA viruses vs. DNA synthesis: a general viral strategy that may contribute to the protective antiviral effects of selenium. Preprints 2020, 2020060069.
  10. Zhang, E.W. Taylor, K. Bennett, R. Saad, M.P. Rayman (2020). Significant association between selenium status and outcome of coronavirus disease, COVID-19. Am. J. Clin. Nutr. 111, 1297-1299.
  11. W. Taylor, W. Radding (2020). Understanding selenium and glutathione as antiviral factors in COVID-19: Does the viral Mpro protease target host selenoproteins and glutathione synthesis? Front. Nutr., In press. doi: 10.3389/fnut.2020.00143.
  12. Wang, J. Huang, Y. Sun, J. He, W. Li, Z. Liu, E.W. Taylor, M.P. Rayman, X. Wan, J. Zhang (2020) SARS-CoV-2 suppresses mRNA expression of selenoproteins associated with ferroptosis, ER stress and DNA synthesis. BioRxiv preprint server, https://doi.org/10.1101/2020.07.31.230243 (submitted to Redox Biology)