MIC Faculty
MIC - Local/NCA Faculty
Christopher C. Broder, Ph.D.
Name: Christopher C. Broder, Ph.D.
USU Department of Primary Appointment:
Microbiology and Immunology
Title:
Professor and Chair
Faculty Rank:
Professor
Location:
Uniformed Services University of the Health Sciences, Bethesda, MD
Research Interests:
Virology; emerging viruses, virus-host cell interactions, vaccines and therapeutics, viral serological surveillance
Basic Biology of Bacterial, Viral, or Parasite Diseases
Email:
Office Phone:
(301) 295-3401
Department Website:
Education
1983 B.S., Biological Sciences, with honors. Florida Institute of Technology, Melbourne, Florida.
1985 M.S., Molecular Biology, Florida Institute of Technology, Melbourne, Florida.
1989 Ph.D., Microbiology and Immunology. College of Medicine, University of Florida, Gainesville, Florida.
1985 M.S., Molecular Biology, Florida Institute of Technology, Melbourne, Florida.
1989 Ph.D., Microbiology and Immunology. College of Medicine, University of Florida, Gainesville, Florida.
Biography
Christopher C. Broder received his B.S. (1983) and M.S. (1985) degrees from the Florida Institute of Technology, Melbourne. He earned his Ph.D. from the University of Florida, Gainesville (1989) establishing a molecular-pathogenic model for the flesh-eating Group A streptococci. He began his postdoctoral studies in 1989 as a National Research Council Research Associate in the Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, focusing on HIV-1 host cell entry and infection. He joined the faculty of the Department of Microbiology and Immunology at Uniformed Services University (USU) as Assistant Professor in 1996 and rose through the ranks to become a full Professor in 2005. His laboratory has focused on virus-host cell interactions with an emphasis on virus receptor discovery, virus entry and virus-mediated membrane fusion, vaccines and antibody therapeutics development. Research areas include HIV-1 and emerging zoonotic viruses including Nipah virus and Hendra virus; Ebola and Marburg viruses, and bat lyssavirus. His major collaborative research contributions include the discoveries of the CXCR4 and the CCR5 HIV-1 coreceptors (1996-Breakthrough of the Year, Science magazine and the AAAS Newcomb Cleveland Prize 1997); the development of the first oligomeric, HIV-1 soluble gp140 glycoprotein vaccine candidate; discovery of the host cell receptor proteins (ephrin ligands) used by Nipah virus and Hendra virus; development of the Hendra/Nipah soluble G glycoprotein subunit vaccine; one formulation known as Equivac® HeV (Zoetis, Inc.), the first commercialized vaccine against a BSL-4 agent. Clinical development of the Hendra soluble G subunit vaccine is underway by Profectus Biosciences, Inc., and supported by CEPI (The Coalition for Epidemic Preparedness Innovations). Therapeutic antiviral human monoclonal antibodies have also been developed, including the anti-Hendra/Nipah human mAb m102.4 which has been used by emergency protocol in 13 people in Australia and one in the U.S. because of significant risk of Hendra or Nipah virus infection. The m102.4 antibody has completed a Phase I clinical trial in Australia, and has recently been supplied to Government of India and included in an international Nipah treatment protocol sponsored by the Indian Council of Medical Research (ICMR) with support from the NIAID, NIH, USA. He currently serves on the editorial board of five journals, and recent honors include the 2019 and 2013 Federal Laboratory Consortium (FLC) Awards for Excellence in Technology Transfer; the CSIRO Chairman’s Medal for 2013, (Australia's national science agency); the 2014 Cinda Helke Award for Excellence in Graduate Student Advocacy and the 2016 James J. Leonard Award for Excellence in Translational/Clinical Research. He has mentored 13 graduate students and 12 postdoctoral scientists, has coauthored more than 165 scientific articles and book chapters and his work has been cited more 19,400 times and is an inventor on 19 US and foreign patents. He served as Director of the Emerging Infectious Diseases Graduate Program at USU from 2006-2018, and his is currently Professor and Chair of the Department of Microbiology and Immunology, USU.
Representative publications, projects, and/or deployments
- Viral serological surveillance in wildlife and livestock:
- Li, Y, Wang, J, Hickey, AC, Zhang, Y, Li, Y, Wu, Y., Zhang, H, Yuan, J, Han, Z, McEachern, J, Broder, CC, Wang, LF, Shi, Z. Antibodies to Nipah or Nipah-like viruses in bats, China. Emerg Infect Dis. 14(12):1974-6 2008.
- Chowdhury S, Khan SU, Crameri G, Epstein JH, Broder CC, Islam A, Peel AJ, Barr J, Daszak P, Wang LF, Luby SP. Serological evidence of henipavirus exposure in cattle, goats and pigs in Bangladesh. PLoS Negl Trop Dis. 2014 Nov 20;8(11):e3302. doi: 10.1371/journal.pntd.0003302. 2014 Nov.
- Lyssavirus-host cell interactions:
- Weir DL, Smith IL, Bossart KN, Wang LF and Broder CC. Host cell infection tropism mediated by Australian bat lyssavirus envelope glycoproteins. Virology, 2013; 444(1-2):21-30. Virology Highlights: http://www.virologyhighlights.com/
- Weir DL, Laing ED, Smith IL, Wang LF, Broder CC. Host cell virus entry mediated by Australian bat lyssavirus G envelope glycoprotein occurs through a clathrin-mediated endocytic pathway that requires actin and Rab5. Virol J. 2014 Feb 27;11(1):40.
- Structural studies on viral envelope glycoproteins:
- Xu K, Rockx B, Xie Y, DeBuysscher BL, Fusco DL, Zhu Z, Chan YP, Feldmann H, Dimitrov DS, Broder CC, and Nikolov DB. Crystal structure of the Hendra virus attachment G glycoprotein complexed with a potent cross-reactive neutralizing human monoclonal antibody. Plos Pathogens, 2013 Oct;9(10):e1003684.
- Xu K, Chan YP, Bradel-Tretheway B, Akyol-Ataman Z, Zhu Y, Dutta S, Yan L, Feng YR, Wang LF, Skiniotis G, Lee B, Zhou ZH, Broder CC*, Aguilar HC* and Nikolov DB*. Crystal structure of the pre-fusion Nipah virus fusion glycoprotein reveals a novel hexamer-of-trimers assembly. PLoS Pathog. 2015 Dec 8;11(12):e1005322. doi: 10.1371/journal.ppat.1005322
Bibliography
Biosketch Link:
- Broder, CC, R Lottenberg, GO vonMering, K. Johnston and MDP Boyle. Isolation of a prokaryotic plasmin receptor: relationship to a plasminogen activator produced by the same microorganism. J. Biol. Chem. 266:4922-28, 1991.
- Broder, CC, DS Dimitrov, R. Blumenthal, and EA Berger. The block to HIV-1 envelope glycoprotein-mediated membrane fusion in animal cells expressing human CD4 can be overcome by a human cell component(s). Virology. 193:483-491, 1993.
- Broder, CC, PL Earl, D Long, B Moss, and RW Doms. Antigenic Implications of HIV-1 Envelope Glycoprotein Quaternary Structure: Oligomer-Specific and -Sensitive mAbs. Proc. Natl. Acad. Sci. USA. 91:11699-11703, 1994.
- Broder, CC and EA Berger. Fusogenic Selectivity of the Envelope Glycoprotein is a Major Determinant of HIV-1 Tropism for CD4+ T-Cell Lines vs. Macrophages. Proc. Natl. Acad. Sci. USA. 92:9004-08, 1995.
- Feng, Y, CC Broder, PE Kennedy, and EA Berger. HIV-1 Entry Cofactor: Functional cDNA Cloning of a Seven-Transmembrane, G Protein-Coupled Receptor. Science. 272:872-877, 1996.
- Bossart, K.N., G. Crameri, A.S. Dimitrov, B.A. Mungall, Y.R. Feng, J.R. Patch, A. Choudhary, L.F. Wang, B.T. Eaton, and C.C. Broder*. Receptor Binding, Fusion Inhibition, and Induction of Cross-Reactive Neutralizing Antibodies by a Soluble G Glycoprotein of Hendra Virus. J. Virol., 79(11):6690-702. 2005.
- Bonaparte, MI, AS Dimitrov, KN Bossart, G Crameri, BA Mungall, KA Bishop, V Choudhry, DS Dimitrov, LF Wang, BT Eaton, and CC Broder*. Ephrin-B2 Ligand is a Functional Receptor for Hendra Virus and Nipah Virus. Proc Natl Acad Sci U S A. 102(30):10652-7. 2005. (from the cover)
- Bossart KN, Rockx B, Feldmann F, Brining D, Scott D, Lacasse R, Geisbert JB, Feng YR, Chan YP, Hickey AC, Broder CC*, Feldmann H, Geisbert TW. A Hendra virus G glycoprotein subunit vaccine protects African green monkeys from Nipah virus challenge. Sci Transl Med. 4(146):146ra107. 2012
- Middleton D, Pallister J, Klein R, Feng YR, Haining J, Arkinstall R, Frazer L, Huang JA, Edwards N, Wareing M, Elhay M, Hashmi Z, Bingham J, Yamada M, Johnson D, White J, Foord A, Heine HG, Marsh GA, Broder CC, Wang LF. Hendra virus vaccine, a one health approach to protecting horse, human, and environmental health. Emerg Infect Dis. 2014 Mar;20(3).
- Geisbert TW*, Mire CE, Geisbert JB, Chan YP, Agans KN, Feldmann F, Fenton KA, Zhu Z, Dimitrov DS, Scott DP, Bossart KN, Feldmann H, Broder CC*. Therapeutic treatment of Nipah virus infection in nonhuman primates with a neutralizing human monoclonal antibody. Sci Transl Med. 2014, 6(242):242ra82.
Stephen J. Davies, B.V.Sc., Ph.D.
Name: Stephen J. Davies, B.V.Sc., Ph.D.
USU Department of Primary Appointment:
Microbiology and Immunology
Faculty Rank:
Associate Professor
Location:
Uniformed Services University of the Health Sciences, Bethesda, MD
Research Interests:
Basic Biology of Bacterial, Viral, or Parasite Diseases
Immunology, Host Defenses
Email:
Office Phone:
(301) 295-3446
Department Website:
Education
B.V.Sc. ~ School of Veterinary Science, University of Bristol, United Kingdom, 1993
Ph.D. ~ College of Veterinary Medicine, Cornell University, United States, 1998
Postdoctoral Fellow ~ Department of Pathology, University of California San Francisco, United States, 1998-2004
Ph.D. ~ College of Veterinary Medicine, Cornell University, United States, 1998
Postdoctoral Fellow ~ Department of Pathology, University of California San Francisco, United States, 1998-2004
Biography
Current Research Interests:
• Elucidation of host factors that modulate schistosome blood fluke development
• Initiation of innate immune responses by schistosomes and other helminths
• Immune evasion by schistosomes and other helminths
• Role of helminth proteases in immune responses to helminths
• Elucidation of helminth signaling pathways that transduce host signals
• Exploitation of helminth protein kinases as novel drug targets
• Mucosal immune responses to Enteroaggregative Escherichia coli
• Elucidation of host factors that modulate schistosome blood fluke development
• Initiation of innate immune responses by schistosomes and other helminths
• Immune evasion by schistosomes and other helminths
• Role of helminth proteases in immune responses to helminths
• Elucidation of helminth signaling pathways that transduce host signals
• Exploitation of helminth protein kinases as novel drug targets
• Mucosal immune responses to Enteroaggregative Escherichia coli
Bibliography
Biosketch Link:
- Riner, D.K., Ferragine, C.E., Maynard, S.K., Davies, S.J. (2013) Regulation of innate responses during pre-patent schistosome infection provides an immune environment permissive for parasite development. PLoS Pathogens 2013;9(10):e1003708. doi: 10.1371/journal.ppat.1003708
- Lamb, E.W., Walls, C.D., Pesce, J.T., Riner, D.K., Maynard, S.K., Crow, E.T., Wynn, T.A., Schaefer, B.C., and Davies, S.J. (2010) Blood fluke exploitation of non-cognate CD4+ T cell help to facilitate parasite development. PLoS Pathogens 6(4):e1000892
- Swierczewski, B.E. and Davies, S.J. (2009) A Schistosome cAMP-Dependent Protein Kinase Catalytic Subunit is Essential for Parasite Viability. PLoS Negl. Trop. Dis. 3(8), e505
- Davies, S.J., Grogan, J.L., Blank R.B., Lim, K.C., Locksley, R.M. and McKerrow, J.H. (2001) Modulation of Blood Fluke Development in the Liver by Hepatic CD4+ Lymphocytes. Science 294, 1358-1361
Kristi L. Frank, Ph.D.
Name: Kristi L. Frank, Ph.D.
USU Department of Primary Appointment:
Microbiology and Immunology
Faculty Rank:
Assistant Professor
Location:
Uniformed Services University of the Health Sciences, Bethesda, MD
Research Interests:
Bacterial pathogenesis and genetics
Treatment and prevention of biofilm infections
Email:
Office Phone:
(301) 295-3415
Department Website:
Education
2002 B.S., Microbiology, B.S., Medical Technology, The University of Montana, Missoula, MT
2007 Ph.D., Biomedical Sciences-Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN
2007 Ph.D., Biomedical Sciences-Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN
Biography
Dr. Kristi L. Frank is an Assistant Professor in the Department of Microbiology and Immunology at Uniformed Services University of the Health Sciences (USU) in Bethesda, MD. A native of Great Falls, MT, she earned her Bachelor of Science degrees in Microbiology and Medical Technology from The University of Montana in Missoula, MT, in 2002. Dr. Frank attended Mayo Graduate School, Mayo Clinic College of Medicine, in Rochester, MN, where she earned her Ph.D. in Biomedical Sciences-Biochemistry and Molecular Biology in 2007. She carried out her dissertation research on Staphylococcus lugdunesis biofilm formation in the laboratory of Dr. Robin Patel. Dr. Frank completed her postdoctoral research in the Department of Microbiology and Immunology at the University of Minnesota in Minneapolis, MN, where she worked with Drs. Gary Dunny and Patrick Schlievert. She joined the faculty at USU in January 2016.
Dr. Frank's lab studies relationships between bacterial pathogens and their hosts in biofilm-associated infections. Biofilms are organized communities of microbes attached to a surface, or to each other, and are encased in a self-produced extracellular matrix. Biofilm growth provides protection from adverse environmental conditions, enables evasion of the host immune defenses, and confers resistance to remarkably high concentrations of antimicrobial agents. Pathogenic bacteria can form biofilms on surfaces throughout a host and on virtually any implantable medical device. Biofilm infections pose a significant challenge to human health because of their chronic nature and the difficulty associated with treating them.
The Frank Lab's current efforts focus on Enterococcus faecalis, a Gram-positive bacterium that is both a human commensal and an opportunistic pathogen. Enterococci are exceptionally robust, recalcitrant to many classes of antimicrobial agents, and highly proficient at acquiring virulence factors via horizontal gene transfer. These characteristics have enabled E. faecalis and other enterococci to emerge as leading causes of healthcare-associated infections. In immunosuppressed patients, E. faecalis can cause a myriad of infections with biofilm etiology, including endocarditis, surgical site infections, and catheter-associated urinary tract infections. The Frank Lab pairs animal models of biofilm formation with genetic, molecular, and biochemical approaches to (1) define sensing pathways and regulatory circuits that are involved in triggering transcriptional and stress responses in the host environment, (2) identify biofilm-associated virulence factors in E. faecalis and determine how they affect interactions between the bacterium and its host, (3) test new methods to remove biofilms and prevent their formation, and (4) pursue the mechanisms by which E. faecalis colonizes endovascular tissues as part of a broader interest in understanding how biofilm-forming bacteria may affect human cardiovascular health.
Dr. Frank's lab studies relationships between bacterial pathogens and their hosts in biofilm-associated infections. Biofilms are organized communities of microbes attached to a surface, or to each other, and are encased in a self-produced extracellular matrix. Biofilm growth provides protection from adverse environmental conditions, enables evasion of the host immune defenses, and confers resistance to remarkably high concentrations of antimicrobial agents. Pathogenic bacteria can form biofilms on surfaces throughout a host and on virtually any implantable medical device. Biofilm infections pose a significant challenge to human health because of their chronic nature and the difficulty associated with treating them.
The Frank Lab's current efforts focus on Enterococcus faecalis, a Gram-positive bacterium that is both a human commensal and an opportunistic pathogen. Enterococci are exceptionally robust, recalcitrant to many classes of antimicrobial agents, and highly proficient at acquiring virulence factors via horizontal gene transfer. These characteristics have enabled E. faecalis and other enterococci to emerge as leading causes of healthcare-associated infections. In immunosuppressed patients, E. faecalis can cause a myriad of infections with biofilm etiology, including endocarditis, surgical site infections, and catheter-associated urinary tract infections. The Frank Lab pairs animal models of biofilm formation with genetic, molecular, and biochemical approaches to (1) define sensing pathways and regulatory circuits that are involved in triggering transcriptional and stress responses in the host environment, (2) identify biofilm-associated virulence factors in E. faecalis and determine how they affect interactions between the bacterium and its host, (3) test new methods to remove biofilms and prevent their formation, and (4) pursue the mechanisms by which E. faecalis colonizes endovascular tissues as part of a broader interest in understanding how biofilm-forming bacteria may affect human cardiovascular health.
Representative publications, projects, and/or deployments
- Frank, K. L., A. M. Barnes, S. M. Grindle, D. A. Manias, P. M. Schlievert, and G. M. Dunny. 2012. Use of recombinase-based in vivo expression technology to characterize Enterococcus faecalis gene expression during infection identifies in vivo-expressed antisense RNAs and implicates the protease Eep in pathogenesis. Infection and Immunity. 80:539-549.
- Frank, K. L., P. S. Guiton, A. M. T. Barnes, D. A. Manias, O. N. Chuang-Smith, P. L. Kohler, A. R. Spaulding, S. J. Hultgren, P. M. Schlievert, and G. M. Dunny. 2013. AhrC and Eep are biofilm infection-associated virulence factors in Enterococcus faecalis. Infection and Immunity. 81:1696-1708.
- Frank, K. L., C. Colomer-Winter, S. M. Grindle, J. A. Lemos, P. M. Schlievert, and G. M. Dunny. 2014. Transcriptome analysis of Enterococcus faecalis during mammalian infection shows cells undergo adaptation and exist in a stringent response state. Plos One. 9:e115839.
- Frank, K. L., P. Vergidis, C. L. Brinkman, K. E. Greenwood-Quaintance, A. M. T. Barnes, J. N. Mandrekar, P. M. Schlievert, G. M. Dunny, and R. Patel. 2015. Evaluation of the Enterococcus faecalis biofilm-associated virulence factors AhrC and Eep in rat foreign body osteomyelitis and in vitro biofilm-associated antimicrobial resistance. Plos One. 10:e0130187.
- Colomer-Winter, C., A. O. Gaca, O. N. Chuang-Smith, J. A. Lemos, and K. L. Frank. 2018. Basal levels of (p)ppGpp differentially affect the pathogenesis of infective endocarditis in Enterococcus faecalis. Microbiology. doi: 10.1099/mic.0.000703
Bibliography
Biosketch Link:
Chou-Zen Giam, Ph.D.
Name: Chou-Zen Giam, Ph.D.
USU Department of Primary Appointment:
Microbiology and Immunology
Title:
Professor and Vice Chair
Faculty Rank:
Professor
Location:
Uniformed Services University of the Health Sciences, Bethesda, MD
Research Interests:
The molecular biology and pathogenesis of human retroviruses and viral oncogenesis. How chronic NF-kB activation promotes genomic instability and cellular senescence.
Email:
Office Phone:
(301) 295-9624
Department Website:
Education
B.S. Chemistry, National Taiwan University, Taipei, Taiwan (05/1975)
Ph. D. Molecular Biology and Biochemistry, University of Connecticut Health Center, Farmington, CT, USA (05/1983)
Post-doctoral Fellow, Laboratory of Molecular Virology, NCI, NIH, Bethesda, MD, USA (09/1987)
Ph. D. Molecular Biology and Biochemistry, University of Connecticut Health Center, Farmington, CT, USA (05/1983)
Post-doctoral Fellow, Laboratory of Molecular Virology, NCI, NIH, Bethesda, MD, USA (09/1987)
Biography
The work in my lab revolves around human viruses, with a special emphasis on human T-cell leukemia virus type 1 (HTLV-1), and with occasional forays into other viruses such as HIV and KSHV. We seek a mechanistic understanding of how viral regulatory proteins hijack cellular mediators of mRNA transcription, cell cycle control, and signal transduction to effect viral replication and pathogenesis, especially, oncogenesis. My interest in cancer viruses and human retroviruses developed initially in the early 1980s in the Laboratory of Molecular Virology (LMV) at the NIH where I was a post-doctoral fellow under the direction of Dr. George Khoury. Our major focus at that time was to understand how transcriptional enhancer elements drive eukaryotic mRNA synthesis by studying the HTLV-1 trans-activator, Tax, and its interaction with the cellular transcription machinery. After leaving LMV for the academia, I have been continuously funded by grants from the NIH and other funding agencies (AmFAR, VA, and DoD). We (and others) have since elucidated the mechanism by which Tax activates viral transcription and contributed to current understanding of how HTLV-1 infects, replicates and causes diseases. Due to the global nature of HTLV-1 infection, we frequently collaborate with colleagues in continental US, Asia (Japan, Taiwan, Hong Kong), Europe (France, UK, Germany, Italy, etc.), Africa (Uganda), and South America (Brazil). Together with our domestic and international partners, we seek fundamental understanding of HTLV-1 replication, persistence, and pathogenesis, and strive to translate basic science findings into preventive measures and therapeutic approaches for HTLV-1-associated diseases, especially adult T cell leukemia (ATL). Our current efforts focus on (1) elucidating the mechanisms that underlie the genomic instability of ATL cells; (2) understanding how the transcriptional activity of NF-B drives the induction of cellular senescence; (3) identifying the genetic alterations in ATL cells that facilitate the clonal expansion of HTLV-1-infected T cells based on whole genome sequence information; and (4) uncovering the mechanisms that regulate HTLV-1 latency and reactivation.
Bibliography
Biosketch Link:
- NF-kB signaling mechanisms in HTLV-1-induced adult T-cell leukemia/lymphoma. Harhaj EW, Giam CZ, FEBS J. 2018. doi: 10.1111/febs.14492.
- HTLV-1 Infection and Adult T-Cell Leukemia/Lymphoma-A Tale of Two Proteins: Tax and HBZ. Giam CZ, Semmes OJ. Viruses. 2016 Jun 16;8(6). pii: E161. https://www.ncbi.nlm.nih.gov/pubmed/27322308
- HTLV-1 Tax Stimulates Ubiquitin E3 Ligase, Ring Finger Protein 8, to Assemble Lysine 63-Linked Polyubiquitin Chains for TAK1 and IKK Activation. Ho YK, Zhi H, Bowlin T, Dorjbal B, Philip S, Zahoor MA, Shih HM, Semmes OJ, Schaefer B, Glover JN, Giam CZ. PLoS Pathog. 2015 Aug 18;11(8):e1005102. https://www.ncbi.nlm.nih.gov/pubmed/26285145
- KSHV vCyclin counters the senescence/G1 arrest response triggered by NF-kB hyperactivation. Zhi H, Zahoor MA, Shudofsky AM, Giam CZ. Oncogene. 2015; 34(4):496-505. NIHMSID: NIHMS550287 https://www.ncbi.nlm.nih.gov/pubmed/24469036
- HTLV-1 tax-induced rapid senescence is driven by the transcriptional activity of NF-kB and depends on chronically activated IKKa and p65/RelA. Ho YK, Zhi H, DeBiaso D, Philip S, Shih HM, Giam CZ. Journal of Virology. 2012; 86(17):9474-83. https://www.ncbi.nlm.nih.gov/pubmed/22740410
- Complex cell cycle abnormalities caused by human T-lymphotropic virus type 1 Tax. Yang L, Kotomura N, Ho YK, Zhi H, Bixler S, Schell MJ, Giam CZ. Journal of Virology. 2011; 85(6):3001-9.
- NF-kB hyper-activation by HTLV-1 tax induces cellular senescence, but can be alleviated by the viral anti-sense protein HBZ. Zhi H, Yang L, Kuo YL, Ho YK, Shih HM, Giam CZ. PLoS pathogens. 2011; 7(4):e1002025. https://www.ncbi.nlm.nih.gov/pubmed/21552325
- Activation of the anaphase promoting complex by HTLV-1 tax leads to senescence. Kuo YL, Giam CZ. The EMBO journal. 2006; 25(8):1741-52. https://www.ncbi.nlm.nih.gov/pubmed/16601696
- Published video: https://www.youtube.com/watch?v=votp2hRndIk&spfreload=10
- Published video: https://www.youtube.com/watch?v=XasVBcMRGls&spfreload=10
Ann E. Jerse, Ph.D.
Name: Ann E. Jerse, Ph.D.
USU Department of Primary Appointment:
Microbiology and Immunology
Title:
Professor
Faculty Rank:
Professor
Location:
Uniformed Services University of the Health Sciences, Bethesda, MD
Research Interests:
Adaptation of Neisseria gonorrhoeae to the female reproductive tract; animal modeling of gonococcal and gonococcal-chlamydial infections; antibiotic resistance and microbial fitness; development of novel anti-infectives and vaccines
Email:
Office Phone:
(301) 295-9629
Department Website:
Education
B.A. Medical Technology, Indiana State University (1979)
Ph.D. Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD, USA (1983)
Post-doctoral Fellow, University of North Carolina, Chapel Hill, NC (1991-1993)
Ph.D. Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD, USA (1983)
Post-doctoral Fellow, University of North Carolina, Chapel Hill, NC (1991-1993)
Representative publications, projects, and/or deployments
- Jerse AE, Wu H, Packiam M, Vonck RA, Begum AA, and LE Garvin. 2011. Estradiol-treated female mice as surrogate hosts for Neisseria gonorrhoeae genital tract infections. Front. Microbio. 2:107. doi: 10.3389.
- Vonck R.A., T. Darville, C.M. O’Connell, and A.E. Jerse. 2011. Chlamydial infection increases gonococcal colonization in a novel murine coinfection model. Infect Immun. 79:1566-1577. PMCID: PMC3067530.
- Muench D.F., Kuch D.J., Wu H., Begum A.A., Veit S.J., Pelletier M. E., Soler-Garcia A.A., and A.E. Jerse. 2009. H2O2-producing lactobacilli inhibit gonococci in vitro but not during experimental genital tract infection. J. Infect. Dis. 199:1369–1378. PMCID: PMC2864085.
- Song W., Condron S., Mocca B.T., Veit S.J., Hill D., Abbas A., and A.E. Jerse. 2008. Local and humoral responses against primary and repeat Neisseria gonorrhoeae genital tract infections of 17-β-estradiol-treated mice. Vaccine 26:5741-5751. PMCID: PMC 2855896.
- Packiam R., H. Wu, S.J. Veit, N. Mavrogiorgios, A.E. Jerse*, and R.R. Ingalls. 2012. Protective role of Toll-like receptor 4 in experimental gonococcal infection of female mice. Mucosal Immunol. 5:19-29. *Co-senior author with RR Ingalls.
- Simms, A.N., and A.E. Jerse. 2006. In vivo selection for Neisseria gonorrhoeae opacity protein expression in the absence of human CEACAM receptors Infect. Immun. 74:2965-2974. PMCID: PMC1459723.
- Warner D.J., W.M. Shafer, and A.E. Jerse. 2008. Clinically relevant mutations that cause derepression of the Neisseria gonorrhoeae MtrC-MtrD-MtrE efflux pump system confer different levels of antimicrobial resistance and in vivo fitness. Mol. Micro. 70:462-478. PMCID: PMC 2602950.
- Kunz A.N., A.A. Begum, H. Wu, J.A. D’Ambrozio, J.M. Robinson, W.M. Shafer, M.C. Bash, and A.E. Jerse. 2012. Impact of fluoroquinolone resistance mutations on gonococcal fitness and in vivo selection for compensatory mutations. J Infect Dis 205:1821-1829.
- Packiam M., Y. Yedery, A.A. Begum, R.W. Carlson, J. Ganguly, G.D. Sempowski, M.S. Ventevogel, W.M. Shafer, and A.E. Jerse. 2014. Phosphoethanolamine decoration of Neisseria gonorrhoeae lipid A plays a dual immunostimulatory and protective role during experimental genital tract infection. Infect. Immun. 82:2170-2179.
- Hobbs M.M., J.E. Anderson, J.T. Balthazar, J.L. Kandler, R.W. Carlson, J. Ganguly, A.A. Begum, J.A. Duncan, J.T. Lin, P.F. Sparling, A.E. Jerse, and W.M. Shafer. 2013. Lipid A structure mediates Neisseria gonorrhoeae fitness during experimental infection of mice and men. mBio 4:e00892-13.
George W. Liechti, Ph.D.
Name: George W. Liechti, Ph.D.
USU Department of Primary Appointment:
Microbiology and Immunology
Faculty Rank:
Assistant Professor
Location:
Uniformed Services University of the Health Sciences, Bethesda, MD
Research Interests:
Basic Biology of Bacterial, Viral, or Parasite Diseases
Molecular Genetics of Bacterial Pathogenesis
Email:
Office Phone:
(301) 295-8138
Department Website:
Education
2012, Ph.D., Microbiology, Immunology, and Cancer Biology, University of Virginia, Charlottesville, VA
2008, M.S., Biology, The College of William and Mary, Williamsburg, VA
2003, B.S., Biology, The College of William and Mary, Williamsburg, VA
2008, M.S., Biology, The College of William and Mary, Williamsburg, VA
2003, B.S., Biology, The College of William and Mary, Williamsburg, VA
Biography
Dr. George Liechti is an Assistant Professor in the Department of Microbiology and Immunology at the Uniformed Services University of the Health Sciences in Bethesda, MD. He obtained his Bachelor of Sciences from The College of William and Mary in 2003 and his Masters of Science in 2008. Dr. Liechti earned his Ph.D. in Microbiology, Immunology, and Cancer Biology in 2012 from the University of Virginia. He conducted his postdoctoral studies at the Uniformed Services University of the Health Sciences from 2012-16 as a Ruth L. Kirschstein National Research Service Award Fellow, and subsequently joined the Department as an Assistant Professor in 2016. Current studies in Dr. Liechti’s laboratory focus on the molecular genetics of bacterial pathogenesis, specifically as it relates to human-adapted microbes. Pathogenic Chlamydia, Borrelia, and Helicobacter species are currently under investigation, specifically the physiological mechanisms that confer persistence to these microbes, allowing them to evade clearance by the host and as well as killing by antibiotic treatment. Dr. Liechti is a contributing member of both the American Society for Microbiology and the Chlamydial Basic Research Society, and is the current faculty advisor to the USUHS Postdoctoral Association.
Bibliography
- Liechti G, Kuru E, Packiam M, Rittichier JT, Tekkam S, Hall E, Hsu Y, VanNieuwenhze M, Brun YV, and Maurelli AT. Pathogenic Chlamydia use a narrow, midcell peptidoglycan ring regulated by MreB for replication. PLOS Pathogens. 2016; 12(5):e1005590. PMID: 27144308
- Liechti G, Kuru E, Hall E, Kalinda A, Brun YV, VanNieuwenhze M, and Maurelli AT. A new metabolic cell wall labeling method reveals peptidoglycan in Chlamydia trachomatis. Nature 2014. Feb 27;506(7489):507-10. PMID: 24336210.
Joseph J. Mattapallil, B.V.Sc., M.S., Ph.D.
Name: Joseph J. Mattapallil, B.V.Sc., M.S., Ph.D.
USU Department of Primary Appointment:
Microbiology and Immunology
Title:
Co-Director of Bench to Bedside and Beyond (BBB) Module and Graduate Molecular Virology (MCO501)
Faculty Rank:
Associate Professor
Location:
Uniformed Services University of the Health Sciences, Bethesda, MD
Research Interests:
Basic Biology of Bacterial, Viral, or Parasite Diseases
Immunology, Host Defenses
Email:
Office Phone:
(301) 295-3737
Department Website:
Education
1997: Ph.D., Immunology, University of California Davis, Davis, CA
1994: M.S., Animal Science, University of California Davis, Davis, CA
1986: B.V.Sc, Veterinary Medicine, College of Veterinary Medicine, APAU, India
1994: M.S., Animal Science, University of California Davis, Davis, CA
1986: B.V.Sc, Veterinary Medicine, College of Veterinary Medicine, APAU, India
Representative publications, projects, and/or deployments
- Standing/Chartered Member, AIDS Immunology and Pathogenesis (AIP) Study Section, Center for Scientific Review, NIH (2014 – 2020)
- Member, DAIT, NIAID Radiation-Nuclear Countermeasures Program Data and Safety Monitoring Committee (RNMC-DSMB), 2011 – 2014
- Member, Over 25 NIH Special Emphasis Panels reviewing AIDS, and Biodefense related grant applications, 2006 – Present
- Associate Editor, Journal of Immunolgy (2013 - present)
- Academic Editor, Plos One (2013 - present)
- Associate Editor, Cellular Immunology (2015 - present)
- Editorial Board Member, Clinical and Vaccine Immunology (2012 - present)
- Editorial Board Member, AIDS Research and Human Retroviruses (2012 - present)
- Ad Hoc Reviewer, Journal of Clinical Investigation, Journal of Infectious Diseases, Mucosal Immunology, Plos Pathogens, FASEB Journal, Blood, Retrovirology, Journal of Virology
Bibliography
- Mattapallil, J., Douek, D. C., Hill, B., Nishimura, Y., Martin, M. A and Roederer, M. 2005. Massive infection and loss of memory CD4 T-cells in multiple tissues during acute SIV Infection. Nature. 434: 1093-97.
- Mattapallil, J., Douek, D.C., Buckler-White, A., Montefiori, D., Letvin, N. L., Nabel, G. J and Roederer, M. 2006. Vaccination prevents the destruction of CD4 memory T cells during acute SIV infection. J. Exp. Med. 203: 1533-41.
- Kader, M., Hassan, W., Eberly, M., Piatak, M., Lifson, J., Roederer, M and Mattapallil, J. J. 2008. Anti-retroviral therapy prior to acute viral replication preserves CD4 T cells in the periphery but not in the rectal mucosa during acute simian immunodeficiency virus infection. J. Virol. 82: 11467-71.
- Eberly, M. D., Kader, M., Hassan, W., Rogers, K. A., Zhou, J., Mueller, Y.M., Mattapallil, M. J., Piatak, M., Lifson, J. D., Katsikis, P. D., Roederer, M., Villinger, F and Mattapallil, J.J. 2009. Increased IL-15 production is associated with higher susceptibility of memory CD4 T cells to SIV during acute infection. J. Immunology. 182: 1439-48.
- Kader, M., Wang, X., Piatak, M., Lifson, J., Roederer, M., Veazy, R and Mattapallil, J. J. 2009. a4+β7hiCD4+ memory T cells harbor most Th-17 cells and are preferentially infected during acute SIV infection. Mucosal Immunology: 2: 439-49.
- Moore, A. C., Bixler, S. L., Lewis, M. G., Verthelyi, D and Mattapallil, J. 2012. Mucosal and Peripheral Lin–HLA-DR+CD11c/123–CD14– Mononuclear cells are preferentially infected very early during simian immunodeficiency virus infection. J Virology: 86: 1069-78.
- Bixler, S., Sandler, N., Douek, D. C. and Mattapallil, J. 2013. Suppressed Th17 levels correlate with elevated PIAS3, SHP2, and SOCS3 Expression in CD4 T cells during acute simian immunodeficiency virus infection. J. Virology: 87: 7093-101.
- Onabajo, O. O., George, J., Lewis, M. and Mattapallil, J. 2013. Rhesus macaque lymph node PD-1hiCD4+ T cells express high levels of CXCR5 and IL-21 and display a CCR7loICOS+Bcl6+ T follicular (Tfh) cell phenotype. Plos One: 8(3):e59758.
- George, J., Lewis, M. G., Renne, R and Mattapallil, J. 2015. Suppression of transforming growth factor b receptor 2 and smad5 is associated with high levels of microRNA miR-155 in the oral mucosa during chronic simian immunodeficiency virus infection. J. Virology: 89: 2972-8.
- George, J., Renn L., Lewis, M. G., Verthelyi, D., Roederer, M., Rabin, R. L. and Mattapallil, J. 2016. Early treatment with reverse transcriptase inhibitors significantly suppresses peak plasma IFNα in vivo during acute simian immunodeficiency virus infection. Cellular Immunology: 310:156-164.
Angela R. Melton-Celsa, Ph.D.
Name: Angela R. Melton-Celsa, Ph.D.
USU Department of Primary Appointment:
Microbiology and Immunology
Faculty Rank:
Associate Professor
Location:
Uniformed Services University of the Health Sciences, Bethesda, MD
Research Interests:
Toxins, Diagnostics, and Therapies
Basic Biology of Bacterial, Viral, or Parasite Diseases
Office Phone:
(301) 295-3649
Department Website:
Education
BS, Loyola Marymount University
Ph.D. Virginia Commonwealth University, Medical College of Virginia
Ph.D. Virginia Commonwealth University, Medical College of Virginia
Bibliography
- Russo LM, Melton-Celsa AR, O'Brien AD. Shiga Toxin (Stx) Type 1a Reduces the Oral Toxicity of Stx Type 2a. J Infect Dis. 2016 Apr 15;213(8):1271-9.
- Melton-Celsa AR, O'Brien AD, Feng PC. Virulence Potential of Activatable Shiga Toxin 2d-Producing Escherichia coli Isolates from Fresh Produce. J Food Prot. 2015 Nov;78(11):2085-8.
- Melton-Celsa AR, O'Brien AD. New Therapeutic Developments against Shiga Toxin-Producing Escherichia coli. Microbiol Spectr. 2014 Oct;2(5). doi: 10.1128/microbiolspec.EHEC-0013-2013.
- Boisen N, Melton-Celsa AR, Scheutz F, O'Brien AD, Nataro JP. Shiga toxin 2a and Enteroaggregative Escherichia coli--a deadly combination. Gut Microbes. 2015 Jul 4;6(4):272-8.
- Melton-Celsa AR, Carvalho HM, Thuning-Roberson C, O'Brien AD. Protective efficacy and pharmacokinetics of human/mouse chimeric anti-Stx1 and anti-Stx2 antibodies in mice. Clin Vaccine Immunol. 2015 Apr;22(4):448-55.
- Melton-Celsa AR. Shiga Toxin (Stx) Classification, Structure, and Function. Microbiol Spectr. 2014 Aug;2(4):EHEC-0024-2013.
- Zangari T, Melton-Celsa AR, Panda A, Smith MA, Tatarov I, De Tolla L, O'Brien AD. Enhanced virulence of the Escherichia coli O157:H7 spinach-associated outbreak strain in two animal models is associated with higher levels of Stx2 production after induction with ciprofloxacin. Infect Immun. 2014 Dec;82(12):4968-77.
- Boisen N, Hansen AM, Melton-Celsa AR, Zangari T, Mortensen NP, Kaper JB, O'Brien AD, Nataro JP. The presence of the pAA plasmid in the German O104:H4 Shiga toxin type 2a (Stx2a)-producing enteroaggregative Escherichia coli strain promotes the translocation of Stx2a across an epithelial cell monolayer. J Infect Dis. 2014 Dec 15;210(12):1909-19.
- Russo LM, Melton-Celsa AR, Smith MA, Smith MJ, O'Brien AD. Oral intoxication of mice with Shiga toxin type 2a (Stx2a) and protection by anti-Stx2a monoclonal antibody 11E10. Infect Immun. 2014 Mar;82(3):1213-21.
- Zumbrun SD, Melton-Celsa AR, O'Brien AD. When a healthy diet turns deadly. Gut Microbes. 2014 Jan-Feb;5(1):40-3.
D. Scott Merrell, Ph.D.
Name: D. Scott Merrell, Ph.D.
USU Department of Primary Appointment:
Microbiology and Immunology
Title:
Professor and Interim Program Director
Faculty Rank:
Professor
Location:
Uniformed Services University of the Health Sciences, Bethesda, MD
Research Interests:
Basic Biology of Bacterial, Viral, or Parasite Diseases
Microbiome, Bacterial stress response and adaptation, Polymicrobial interactions
Email:
Office Phone:
(301) 295-1584
Department Website:
Education
1988-1992 B.S. Biology magna cum laude, Lyon College
1994-1996 M.S. Microbiology, University of Arkansas, Advisor: Mack Ivey, Ph.D.
1996-2001 Ph.D. Molecular Biology and Microbiology, Tufts University School of Medicine, Advisor: Andrew Camilli, Ph.D.
2001-2004 Postdoctoral Fellow, Stanford School of Medicine, Advisor: Stanley Falkow, Ph.D.
1994-1996 M.S. Microbiology, University of Arkansas, Advisor: Mack Ivey, Ph.D.
1996-2001 Ph.D. Molecular Biology and Microbiology, Tufts University School of Medicine, Advisor: Andrew Camilli, Ph.D.
2001-2004 Postdoctoral Fellow, Stanford School of Medicine, Advisor: Stanley Falkow, Ph.D.
Biography
D. Scott Merrell (Scotty) was born and raised in rural Bald Knob, Arkansas but left the south to complete his Ph.D. studies at Tufts Medical School. While there he conducted studies that were focused on understanding the role of the acid tolerance response in the ability of Vibrio cholerae to successfully colonize the human host. After completing his Ph.D. in 2001, he moved to Stanford University, where he completed a postdoctoral fellowship, which focused on utilization of genomic techniques to understand the stress response of the gastric pathogen Helicobacter pylori. He is currently a Professor in the Department of Microbiology and Immunology at Uniformed Services University in Bethesda, Maryland. Scotty is a former “Applied Genomics of Infectious Diseases,” ID Training Fellow, a Damon Runyon-Walter Winchell Cancer Fund Postdoctoral Fellow and received a Merck Irving S. Sigal Memorial Award for excellence in basic research in medical microbiology and infectious diseases in 2008. Scotty’s research group currently studies colonization and virulence factors of the gastric pathogen H. pylori, the microbiome associated with S. aureus infection, S. aureus resistance and polymicrobial interactions, and stress response in A. baumannii.
Representative publications, projects, and/or deployments
- 2008, Merck Irving S. Sigal Memorial Award for excellence in basic research in medical microbiology and infectious diseases.
- 2012-2014, ASM Branch Lectureship
- 2015, Cinda Helke Award for Excellence in Graduate Student Advocacy
- 2015, F. Edward Hébert School of Medicine Impact Award
- 2014-present, Graduate Education Chair
- 2007-present, EID Graduate Program Executive Committee
- 2007-present, Biomedical Instrumentation Advisory Committee
- 2010-present, Associate Editor Frontiers in Cellular and Infection Microbiology
- 2006-present, Member, Editorial Board Infection and Immunity
- 2017-2020, Member, Editorial Board International Journal of Medical Microbiology
Bibliography
Biosketch Link:
- D.S. Merrell, S.M. Butler, F. Qadri, N. A. Dolganov, A. Alam, M.B. Cohen, S.B. Calderwood, G.K. Schoolnik, and A. Camilli. “Host Induced Epidemic Spread of the Cholera Bacterium.” Nature 417(6889):642-645, 2002. PMC2776822
- D.R. Bridge, J.M. Whitmire, J.J. Gilbreath, E.S. Metcalf, and D.S. Merrell. "An Enterobacterial Common Antigen Mutant of Salmonella enterica serovar Typhimurium as a Vaccine Candidate." International Journal of Medical Microbiology, Sep;305(6):511-22. doi: 10.1016/j.ijmm.2015.05.004, 2015.
- R.C. Johnson, C.D. Schlett, K. Crawford, J.B. Lanier, D.S. Merrell, and M.W. Ellis. “Recurrent Methicillin-resistant Staphylococcus aureus Cutaneous Abscesses and the Selection of Reduced Chlorhexidine Susceptibility During Chlorhexidine Use.” Journal of Clinical Microbiology, Nov;53(11):3677-82. doi: 10.1128/JCM.01771-15, 2015.
- A. Kim, S.L. Servetas, J. Kang, J. Kim, S. Jang, H.J. Cha, W.J. Lee, J. Kim, J. Romero-Gallo, R.M. Peek Jr. D.S. Merrell*, and J.H. Cha “Helicobacter pylori bab Paralog Distribution and Association with cagA, vacA, and homA/B genotypes in American and South Korean Clinical Isolates.” PLoS ONE, Aug 28;10(8):e0137078. doi: 10.1371/journal.pone.0137078, 2015.
- A.S. Lo, D.S. Merrell, H. Lei, A. Sardi, T. McAvoy, and T.L. Testerman. "A Novel Member of Chitinophagaceae Isolated from a Human Peritoneal Tumor." Genome Announcements, Nov 12;3(6). pii: e01297-15. doi: 10.1128/genomeA.01297-15, 2015.
- C.L. Williams, H.M. NEU, J.J. Gilbreath, S.L. Michel, D.V. Zurawski and D.S. Merrell. “Copper Resistance of the Emerging Pathogen Acinetobacter baumannii.” Applied and Environmental Microbiology, 82(20):6174-6188, 2016.
- J. Singh, R.C. Johnson, C.D. Schlett, E.M. Elassal, K.B. Crawford, D. Mor, J.B. Lanier, N.N. Law, W.A. Walters, N. Teneza-Mora, J.W. Bennett, E.R. Hall, E.V. Millar, M.W. Ellis, and D.S. Merrell. “Multi-Body Site Microbiome and Culture Profiling of Military Trainees Suffering From Skin and Soft-Tissue Infections at Fort Benning, GA.” mSphere, Oct 5;1(5), 2016. pii: e00232-16.
- R.C. Johnson, M.W. Ellis, C.D. Schlett, E.V. Millar, P.T. LaBreck, D. Mor, E.M. Elassal, J.B. Lanier, C.L. Redden, T. Cui, N. Teneza-Mora, D.K. Bishop, E.R. Hall, K.A. Bishop-Lilly, and D.S. Merrell. “Bacterial Etiology and Risk Factors Associated with Cellulitis and Purulent Skin Abscesses in Military Trainees.” PLoS ONE, Oct 25;11(10):e0165491. doi: 10.1371/journal.pone.0165491.
Edward Mitre, M.D.
Name: Edward Mitre, M.D.
USU Department of Primary Appointment:
Microbiology and Immunology
Faculty Rank:
Professor
Location:
Uniformed Services University of the Health Sciences, Bethesda, MD
Research Interests:
Immunology, Host Defenses
Basic Biology of Bacterial, Viral, or Parasite Diseases
Email:
Office Phone:
(301) 295-1958
Department Website:
Education
2001 Infectious Diseases Fellowship, NIAID, NIH, Bethesda, MD
1998 Internal Medicine Residency, New York University, New York, NY
1995 M.D., Johns Hopkins University School of Medicine, Baltimore,
1991 B.A., Biology, Columbia University, New York, NY
1998 Internal Medicine Residency, New York University, New York, NY
1995 M.D., Johns Hopkins University School of Medicine, Baltimore,
1991 B.A., Biology, Columbia University, New York, NY
Biography
Edward Mitre is a Professor in the Department of Microbiology and Immunology at the Uniformed Services University in Bethesda, Maryland. He obtained his medical degree from the Johns Hopkins School of Medicine in 1995 and then completed an internal medicine residency at New York University. He then did an infectious diseases fellowship at the National Institutes of Health, followed by post-doctoral research work in helminth immunology as well as clinical training in tropical medicine at the Laboratory of Parasitic Diseases at the NIH. Dr. Mitre’s laboratory studies the biology, immunology, and pathogenesis of filarial infections and allergic diseases. Filariae are tissue-invasive nematodes that cause diseases such as elephantiasis and river blindness. Current studies in Dr. Mitre’s laboratory are focused on identifying novel drug and vaccine targets in filarial nematodes, evaluating natural products for the treatment of filariae, developing helminth-derived therapies for allergy and autoimmunity, and elucidating the mechanisms that drive immunoregulation in chronic helminth infections and allergy immunotherapy. In addition to his laboratory research and teaching responsibilities at the Uniformed Services University, Dr. Mitre regularly attends on the internal medicine and infectious diseases services at the Walter Reed National Military Medical Center.
Representative publications, projects, and/or deployments
- Morris, C.P., Bennuru, S., Kropp, L.E., Zweben, J.A., Meng, Z., Taylor, R.T., Chan, K., Veenstra, T.D., Nutman, T.B., and Mitre, E., “A proteomic analysis of the body wall, digestive tract, and reproductive tract of Brugia malayi.” PLoS Neglected Tropical Diseases, 2015, 9(9):e0004054.
- Evans, H., Killoran, K.E., Mitre, B.K., Smith, M.A., Morris, C.P., Kim, S. and Mitre, E. “Ten weeks of infection with a tissue-invasive helminth protects against immune complex-mediated inflammation but not clinical type I hypersensitivity in previously sensitized mice.” Journal of Immunology, 2015, 195(7):2973-84.
- Fox, E.M., Torrero, M., Evans, H., and Mitre, E. “Immunologic characterization of three murine regimens of allergen-specific immunotherapy.” Journal of Allergy and Clinical Immunology, 2015, 135(5):1341-51.
- Evans, H. and Mitre, E., “Worms as therapeutics for allergy: understanding why benefits in animal studies have not translated into clinical success.” Journal of Allergy and Clinical Immunology, 2015, 135(2):343-53.
Bibliography
Biosketch Link:
- Commendation Letter from Major General Jeffrey B. Clark, U.S. Army, on behalf of Walter Reed National Military Medical Center, “For meritorious service while serving as a health care provider to a critically ill and complex patient in the Medical ICU" 2016
- Outstanding Lecturer of the Preclinical Years (USU SOM classes of 2009, 2012, 2016-18)
- Outstanding Civilian Educator Award, USU SOM class of 2016
- Chair, American Society of Tropical Medicine and Hygiene Young Investigator Competition 2016-present (member and judge, 2008-15)
- Associate Editor PLoS Pathogens 2014-present
- Chair, Filariasis Section, American Society of Tropical Medicine and Hygiene Annual Meeting Committee, 2010-2013 (member 2007-2009)
- Senior Chief Resident in Internal Medicine, New York University, 1998-1999
Brian C. Schaefer, Ph.D.
Name: Brian C. Schaefer, Ph.D.
USU Department of Primary Appointment:
Microbiology and Immunology
Faculty Rank:
Professor
Location:
Uniformed Services University of the Health Sciences, Bethesda, MD
Research Interests:
Immunology, Host Defenses
Cell Mechanisms of Disease, Cell Injury and Repair
Email:
Office Phone:
(301) 295-3402
Department Website:
Education
Ph.D. in Immunology, Harvard University, Cambridge, MA, 1995
B.S. in Biology, Massachusetts Institute of Technology, Cambridge, MA, 1989
B.S. in Biology, Massachusetts Institute of Technology, Cambridge, MA, 1989
Biography
Dr. Brian C. Schaefer is a Professor in the Department of Microbiology and Immunology at the Uniformed Services University (USU) in Bethesda, MD. He also holds secondary appointments as Professor in the following USU graduate (Ph.D.) programs: Emerging Infectious Diseases; Molecular and Cell Biology; and Neuroscience. Dr. Schaefer received his B.S. in Biology from the Massachusetts Institute of Technology in Cambridge, MA in 1989. He then performed doctoral studies at Harvard University, where he was awarded his Ph.D. in Immunology in 1995. His dissertation project was performed with Drs. Samuel Speck and Jack Strominger, investigating the molecular basis of a restricted program of Epstein-Barr virus (EBV) gene expression in Burkitt lymphoma. After a brief post-doctoral term with Drs. Speck and Strominger, Dr. Schaefer performed post-doctoral studies (1996 - 2002) with Drs. Philippa Marrack and John Kappler, investigating mechanisms of T cell receptor (TCR) signal transduction. Upon starting his faculty position at USU in 2002, Dr. Schaefer's initial research focus was defining molecular mechanisms by which the TCR transduces signals to the transcription factor, NF-kappaB. This project remains a major emphasis in his research program. Additional areas of active investigation now include defining the role of the inflammatory response in the central nervous system in response to traumatic brain injury (TBI) and viral infection; developing new therapeutic strategies to combat neurotropic viral infections; determining the role of myeloid cells in establishing local immunosuppression in lung adenocarcinoma; and elucidating molecular mechanisms that regulate cell death in myeloid cells. Dr. Schaefer has several NIH- and DoD-funded projects on the above topic areas, with collaborators at USU, the NIH, the Murtha Cancer Center (MCC) at the Walter Reed National Military Medical Center (WRNMMC), the University of Maryland, Duke University Medical Center and the Inova Health System. Dr. Schaefer's honors and awards include the USU Henry Wu Award for excellence in basic science research (2016), a competitive research award from the Dana Foundation Program in Brain and Immuno-imaging (2005) and a Kimmel Scholar Award (2004).
Representative publications, projects, and/or deployments
- Uniformed Services University Biomedical Instrumentation Center (BIC) Faculty Advisory Committee – Chair, 2009 - present
- National Institutes of Health CMIB (Cell and Molecular Immunology-B) study section, ad hoc member, 2011 - current
- Frontiers in Cell and Developmental Biology Cell Death and Survival Section, Editorial Board, 2013 - current
Bibliography
Biosketch Link:
- Traver M, Paul S and Schaefer BC. T cell receptor activation of NF-κB in effector T cells: visualizing signaling events within and beyond the cytoplasmic domain of the immunological synapse. The Immune Synapse: Methods and Protocols, Methods in Molecular Biology, Cosima T. Baldari and Michael L. Dustin (ed.), 2017; 1584:101- 127.
- Lagraoui M, Sukumar G, Latoche JR, Maynard S, Dalgard CL, and Schaefer BC. Salsalate treatment following traumatic brain injury reduces inflammation and promotes a neuroprotective and neurogenic transcriptional response with concomitant functional recovery. Brain, Behavior and Immunity, 2017; 61:96-109.
- Paul S and Schaefer BC. Visualizing TCR-Induced POLKADOTS Formation and NF-κB Activation in the D10 T-Cell Clone and Mouse Primary Effector T Cells. NF-κB: Methods and Protocols, Methods in Molecular Biology, Michael J. May (ed.), 2015; 1280:219- 38.
- Paul S, Traver MK, Kashyap AK, Washington MA, Latoche JR, and Schaefer BC. T cell receptor signals to NF-kappaB are transmitted by a cytosolic p62-Bcl10-Malt1-IKK signalosome. Science Signaling. 2014; 7:ra45.
- Paul S, Kashyap AK, Jia W, He Y-W, Schaefer BC. Selective autophagy of the adaptor protein Bcl10 modulates T cell receptor activation of NF-kappaB. Immunity. 2012; 36:947-58.
- Lagraoui M, Latoche JR, Cartwright NG, Sukumar G, Dalgard CL, Schaefer BC. Controlled cortical impact and craniotomy induce strikingly similar profiles of inflammatory gene expression, but with distinct kinetics. Front Neurol. 2012; 3:155.
- Kingeter LM, Paul S, Maynard SK, Cartwright NG, and Schaefer BC. Cutting Edge: T cell receptor ligation triggers digital activation of NF-kappaB. J. Immunol. 2010; 185:4520-4.
- Langel FD, Jain NA, Rossman JS, Kingeter LM, Kashyap AK, and Schaefer BC. Multiple protein domains mediate interaction between Bcl10 and Malt1. J. Biol. Chem. 2008; 283: 32419-31.
- Kingeter LM and Schaefer BC. Loss of PKCθ, Bcl10, or Malt1 selectively impairs proliferation and NF-κB activation in the CD4+ T cell subset. J. Immunol. 2008; 181:6244-54.
- Rossman JS, Stoicheva NG, Langel FD, Patterson GH, Lippincott-Schwartz J, and Schaefer BC. POLKADOTS are foci of functional interactions between cytosolic intermediates in T cell receptor-induced activation of NF-kappaB. Mol. Biol. Cell 2006; 17:2166-76.
Kim C. Williamson, Ph.D.
Name: Kim C. Williamson, Ph.D.
USU Department of Primary Appointment:
Microbiology and Immunology
Faculty Rank:
Professor
Location:
Uniformed Services University of the Health Sciences, Bethesda, MD
Research Interests:
Basic Biology of Bacterial, Viral, or Parasite Diseases
Immunology, Host Defenses
Email:
Office Phone:
(301) 295-3951
Department Website:
Education
PhD, Boston University
BS, Ithaca College
BS, Ithaca College
Biography
Kim C. Williamson recently joined the Uniformed Services University of the Health Sciences Faculty as a Professor in the Microbiology and Immunology Department. Her primary research interests are malaria immunity and transmission. Specific projects include developing malaria drugs and vaccines as well as studying the basic biology of parasite differentiation in vitro and in vivo in Ghana. She received a Ph.D. from Boston University and started working on malaria as a post-doctoral fellow at the National Institutes of Health in the Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases. After her fellowship she joined the faculty at Loyola University Chicago, where she taught and did research before moving to USUHS. Dr. Williamson is also on the editorial board of Parasitology Research and a member of the American Society for Tropical Medicine and Hygiene and the malERA Refresh Panel.
Bibliography
Biosketch Link:
