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Gene S. Tan, Ph.D.
Assistant Professor

Research Interests and Accomplishments

Gene Tan is an assistant professor at the J. Craig Venter Institute working in the Infectious Disease group. The focus of his research is on virus-host interactions by defining the immunological, molecular and genetic determinants that govern immunity and disease. The aim is to better understand how viruses manipulate the host machinery to replicate and in turn elucidate the mechanisms by which the host counteracts the pathogen. Analyses of virus-host interaction can then facilitate the development of better diagnostic tools, novel therapeutics and vaccines.

Prior to his appointment at JCVI, Dr. Tan was a post-doctoral fellow at the Icahn School of Medicine at Mount Sinai working on characterizing the immunological and structural determinants of protection against influenza virus and Zika virus. He received his doctorate from Thomas Jefferson University and his undergraduate degree from the Philadelphia College of Pharmacy and Science.

Research Priorities

Characterization of the structural and immunological determinants of protection against viral pathogens:

  • Elucidate the mechanisms by which antibodies neutralize virus and protect in vivo.
  • Emphasis on developing novel methods in isolating monoclonal antibodies from human peripheral blood mononuclear cell (PBMC) compartment.

Characterization of virus-host interaction by defining the molecular and transcriptional response

  • Emphasis on respiratory and neurotropic pathogens.


Vaccines for use in the prophylaxis and treatment of influenza virus disease (Pat. No. US20170114103)

Select Publications

He W, Tan GS, et al.
Epitope Specificity Plays a Critical Role in Regulating Antibody-dependent Cell-mediated Cytotoxicity Against Influenza A Virus.

Proceedings of the National Academy of Sciences of the United States of America. 2016 Oct 18; 113. : 11931-11936.[more]

Leon PE, He W, et al.
Optimal Activation of Fc-mediated Effector Functions by Influenza Virus Hemagglutinin Antibodies Requires Two Points of Contact.

Proceedings of the National Academy of Sciences of the United States of America. 2016 Oct 04; 113. : E5944-E5951.[more]

Henry Dunand CJ, Leon PE, et al.
Both Neutralizing and Non-Neutralizing Human H7N9 Influenza Vaccine-Induced Monoclonal Antibodies Confer Protection.

Cell Host & Microbe. 2016 Jun 08; 19. : 800-13.[more]

Tan GS, Leon PE, et al.
Broadly-Reactive Neutralizing and Non-neutralizing Antibodies Directed Against the H7 Influenza Virus Hemagglutinin Reveal Divergent Mechanisms of Protection.

PLoS Pathogens. 2016 Apr 01; 12. : e1005578.[more]

Chen CJ, Ermler ME, et al.
Influenza A Viruses Expressing Intra- or Intergroup Chimeric Hemagglutinins.

Journal of Virology. 2016 Jan 13; 90. : 3789-93.[more]

Leyva-Grado VH, Tan GS, et al.
Direct Administration in the Respiratory Tract Improves Efficacy of Broadly Neutralizing Anti-influenza Virus Monoclonal Antibodies.

Antimicrobial Agents and Chemotherapy. 2015 Jul 01; 59. : 4162-72.[more]

Henry Dunand CJ, Leon PE, et al.
Preexisting Human Antibodies Neutralize Recently Emerged H7N9 Influenza Strains.

The Journal of Clinical Investigation. 2015 Mar 02; 125. : 1255-68.[more]

Tan GS, Lee PS, et al.
Characterization of a Broadly Neutralizing Monoclonal Antibody That Targets the Fusion Domain of Group 2 Influenza A Virus Hemagglutinin.

Journal of Virology. 2014 Dec 01; 88. : 13580-92.[more]

DiLillo DJ, Tan GS, et al.
Broadly Neutralizing Hemagglutinin Stalk-specific Antibodies Require FcγR Interactions for Protection Against Influenza Virus in Vivo.

Nature Medicine. 2014 Feb 01; 20. : 143-51.[more]

Tan GS, Krammer F, et al.
A Pan-H1 Anti-hemagglutinin Monoclonal Antibody With Potent Broad-spectrum Efficacy in Vivo.

Journal of Virology. 2012 Jun 01; 86. : 6179-88.[more]

Tan GS, Preuss MA, et al.
The Dynein Light Chain 8 Binding Motif of Rabies Virus Phosphoprotein Promotes Efficient Viral Transcription.

Proceedings of the National Academy of Sciences of the United States of America. 2007 Apr 24; 104. : 7229-34.[more]

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