Research Assistant Professor: Tadahisa Teramoto

 

Tadahisa Teramoto

 

Dr. Tadahisa Teramoto is an Assistant Research Professor at the Department of Microbiology & Immunology. Dr. Teramoto received his M.D. from Tottori University School of Medicine and Ph.D. from Kobe University School of Medicine, Japan. His postdoctoral training was in the Laboratory of Experimental Carcinogenesis at National Cancer Institute. Since 2001, his research has been focused on understanding the basic mechanisms of viral replication and assembly of mosquito- borne flaviviruses focusing on dengue, West Nile and Zika viruses. These viruses are globally important human pathogens which infect over 300 million humans annually. Ongoing research also focuses on how Wolbachia symbiont interferes with the flavivirus life cycle as well as development of therapeutics against these viruses.

Summary
  • M.D.: Tottori University School of Medicine, Japan; 1988
  • Ph.D.: Kobe University School of Medicine, Japan; 1994
  • Postdoctoral Fellow: National Cancer Institute, Lab of Experimental Carcinogenesis; 2000
  • Research Associate: University of Kansas Medical Center; 2001-2002
  • Research Associate: Georgetown University Medical Center; 2002-2018
  • Assistant Research Professor: Georgetown University Medical Center; 2019-present
  • Training students: Training of Ph.D. rotation students and M.S. degree interns as well as undergraduate and high school students
  • Contact: 202-687-6546; tt54@georgetown.edu
Current Research

Mosquito-transmitted flaviviruses include globally important human pathogens such as dengue, yellow fever, West Nile, and Zika viruses. They have genomes coding for 10 proteins. Viral replication occurs in the cytoplasm of infected host cells. The 5’-end is capped and 3’-end has no poly(A). The positive sense viral RNA is translated into a polyprotein that is processed into 3 structural proteins forming the virion and seven proteins, involved in replication, assembly, and evasion of host immune response. The focus of my lab is to understand the mechanisms of how the multi-functional proteins, NS3 and NS5, are involved in the virus replication and assembly. Our recent focus is on understanding the mechanism(s) of how the bacterial symbiont, Wolbachia, is able to block virus transmission from mosquitoes to humans.

Publications
  • Teramoto T, Kohno Y, Mattoo P, Markoff L, Falgout B, and Padmanabhan R. Genome 3’ end repair in dengue virus type 2. RNA 14(12): 2645-56, 2008. PMCID: PMC2590968
     
  • Teramoto T, Boonyasuppayakorn S, Handley M, Choi KH, Padmanabhan R. Substitution of NS5 N-terminal domain of dengue virus type 2 RNA with type 4 domain caused impaired replication and emergence of adaptive mutants with enhanced fitness. J Biol Chem. 289(32): 22385-400, 2014. PMCID:PMC4139246

  • Klema VJ, Ye M, Hindupur A, Teramoto T, Gottipati K, Padmanabhan R, Choi KH. Dengue Virus Nonstructural Protein 5 (NS5) Assembles into a Dimer with a Unique Methyltransferase and Polymerase Interface. PLoS Pathog. 12(2):e1005451, 2016. PubMed PMID: 26895240; PubMed Central PMCID: PMC4760774.

  • Teramoto T, Balasubramanian A, Choi KH, Padmanabhan R. Serotype-specific interactions among functional domains of dengue virus 2 nonstructural proteins (NS) 5 and NS3 are crucial for viral RNA replication. J Biol Chem. 2017 Jun 9;292(23):9465-9479. doi: 10.1074/jbc.M117.775643.

  • Teramoto T, Huang X, Armbruster PA, Padmanabhan R. Infection of Aedes albopictus Mosquito C6/36 Cells with the wMelpop Strain of Wolbachia Modulates Dengue Virus-Induced Host Cellular Transcripts and Induces Critical Sequence Alterations in the Dengue Viral Genome. J Virol. 2019 Aug 1;93(15). doi: 10.1128/JVI.00581-19. Print 2019 Aug 1. PubMed PMID: 31092581; PubMed Central PMCID: PMC6639269

For a complete list of publications in Pubmed, please click this link: http://www.ncbi.nlm.nih.gov/myncbi/collections/bibliography/49590419/