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Faculty Information

David N. Levy, Ph.D.
Associate Professor
Basic Science and Craniofacial Biology
Room 921 Dental Center, 421 First Avenue
Fax: 212-995-3250



1985, B.A., Biology, Williams College, Williamstown, MA

1994 Ph.D., Immunology, University of Pennsylvania, Philadelphia, PA


Research Interests / Professional Overview:

Office Phone: 212 998-9287, Lab: 212 998-9276 

My laboratory studies the replication, pathogenesis and immunology of the human immunodeficiency virus (HIV).

Two areas of particular interest are the interactions between virus strains as a result of multiple infection of cells and the contribution of unintegrated viruses to HIV replication, diversification and immunology.

Unintegrated HIV. As member of the retrovirus family of viruses, HIV must integrate its DNA into the DNA of the cells which it infects. However, this process is prone to failure, resulting in the great majority of HIV DNA, up to 99%, remaining in an unintegrated state within cells. We have defined a novel pathway for HIV replication which involves unintegrated HIV DNA and which promotes virus evolution, persistence and disease. This work is funded by a 5 year R01 grant from the National Institute of Allergy and Infectious Diseases at the NIH.

Multiple infection and viral interactions. When a cell is infected with more than one virions, there are several consequences which can be of benefit or harm to the virus and the host. Firstly, genetic recombination between divergent viruses contributes to HIV evolution, the emergence of drug resistance and immune escape. Secondly, the viruses can influence each other directly, increasing virus expression, decreasing latency and increasing cell death. Thirdly, the presentation of viral antigens to the immune system can be altered. Using a variety of cellular, molecular and immunological techniques, many of which are unique to my laboratory, we are studying each of these processes and their contributions to the replication and pathogenesis of HIV.

Modeling HIV replication. In collaboration with Dr. Dominik Wodarz, University of California, Irvine, we are applying the knowledge gained from our laboratory experiments to the development of quantitative models of HIV replication, pathogenesis and immunology. We are co-PIs on a 4 year NIH/NIAID R01 grant to study how multiple infection of cells influences viral replication dynamics.


I am the Director of the NYUCD Flow Cytometry Core Facility.


Current Funding:

HIV-1 Replication without integration. NIH/NIAID R01 

Virus Dynamics and Multiple Infection of Cells: Computational and Experimental Analysis. NIH/NIAID/NIGMS R01


Pub Med Articles:

Levy DN


Representative Publications:

 Komarova, N. L., Anghelina, D., Voznesensky, I., Trinité, B., Levy, D. N. and D. Wodarz. (2013) Relative contribution of free virus and synaptic transmission to the spread of HIV through target cell populations. Biol. Letters. 9:20121049.

Komarova, N. L., Levy, D. N. and D. Wodarz. (2012) Effect of synaptic transmission on viral fitness in HIV infection. PLoS One. 7(11):e48361.

Cummings, K. W., Levy, D. N. D. Wodarz. (2012). Increased burst size in multiply infected cells alters basic infection dynamics. Biology Direct. 7:16.

Meditz, A. L., Haas, M. K., Folkvord, J. M., Melander, K., Young, R., McCarter, M., MaWhinney, S., Campbell, T., Weinberg, A., Coakley, E., Levy, D. N., E. Connick. (2011). HLA-DR+CD38+ T Lymphocytes Express High Levels of CCR5 and Produce the Majority of R5-tropic HIV-1 in Human Lymph Nodes. Journal of Virology. J Virol. 85:10189-200

Wodarz, D. and D. N. Levy. (2011). Effect of multiple infection of cells on the evolutionary dynamics of HIV in vivo: implications for host adaptation mechanisms. Experimental Biology and Medicine. 236: 926–937.

Del Portillo, A., Tripodi, J., Najfeld, V., Wodarz, D., D. N. Levy. , B. K. Chen. (2011). Multiploid inheritance of HIV-1 during cell-to-cell infection. Journal of Virology, 85:7169–7176.

Wodarz, D. and D. N. Levy. (2010) Effect of different modes of viral spread on the dynamics of multiply infected cells in human immunodeficiency virus infection. Journal of the Royal Society Interface. 8:289-300.

Bansal, A., Carlson, J., Yan, J., Olusimidele, T. A., Schaefer, M., Sabbaj, S., Bet, A.,Levy, D. N., Heath, S., Walker, B. D., Ndung'u, T., Goulder, P. J., Heckerman, D., Hunter, E., P. A. Goepfert. (2010). CTL response and evolutionary changes to HIV-1 cryptic epitopes derived from antisense transcription. J. Exp. Med. 207:51-59.

Hioe, C., Visciano, M. L., Kuman, R., Liu, J., Levy, D. N., Tuen, M. (2009). The use of immune complex vaccines to enhance antibody response against neutralizing epitopes on HIV-1 envelope gp120. Vaccine. 28:352-360.

Wodarz, D. and D. N. Levy. (2009) Multiple infection of cells and the evolutionary dynamics of cytotoxic T lymphocyte escape mutants. Evolution. 63:2326-2339.

Gelderblom, H. C., , Vatakis, D., Burke, S. A., Lawrie, S., Bristol, G. A., D. N. Levy.(2008) Viral complementation allows HIV-1 replication without integration. Retrovirology. 5:60.

     Commentary on Gelderblom et al. in Retrovirology.

Wodarz, D. and D. N. Levy. (2007) HIV coinfection and viral evolution towards reduced replicative fitness: a requirement for the development of AIDS? Proc. Royal Soc. B. 274:2481-2490.

Decker, J. M., Bibollet-Ruche, F., Wei, X., Wang, S., Levy, D. N., Derdeyn, C. A., Allen, S., Hunter, E., Saag, M. S., Hoxie, J., Hahn, B. H., Kwong, P. D., Robinson, J. E., and G. M. Shaw. (2005) Antigenic Conservation and Immunogenicity of the HIV Co-Receptor Binding Site. J. Exp. Med. 201:1407-1419.

Kutsch, O., Levy, D. N., Bates, P. J., Decker, J., Kosloff, B. R., Shaw, G. M., Priebe, W., and E. N. Benveniste. (2004). Bis-anthracycline antibiotics target HIV-1 tat transactivation. Antimicrob. Agents Chemother. 48:1652-1663.

Levy, D. N., Aldrovandi, G. M., Kutsch, O., and G. M. Shaw. (2004). Dynamics of HIV-1 recombination in its natural target cells. Proc. Natl. Acad. Sci. USA. 101:4204-4209.

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Gao, F., Chen, Y., Levy, D. N., Conway, J. A., Kepler, T. B., and H. Hui. (2004). Unselected mutations in the human immunodeficiency virus type 1 genome are mostly non-synonymous and often deleterious. J. Virol. 78:2426-2433.

Kutsch, O., Levy, D. N., Kosloff, B. R., Shaw, G. M., and E. N. Beneveniste. (2003).
CD154-CD40 induced reactivation of latent HIV-1. Virology. 314:261-270.

Kutsch, O., Beneveniste, E. N., Shaw, G. M., and Levy, D. N. (2002). Direct and quantitative single-cell analysis of human immunodeficiency virus type 1 reactivation from latency. J. Virol. 76:8776-8786.

Agadjanyan, M. G., Trivedi, N. N., Kudchodkar, S., Bennet, M., Levine, W., Lin, A., Boyer, J. , Levy, D., Ugen, K. E. , Kim, J. J., and Weiner, D. B. (1997). An HIV type 2 DNA vaccine induces cross-reactive immune responses against HIV type 2 and SIV. AIDS Res. Hum. Retroviruses. 13:1561-1572.

Refaeli, Y., Levy, D. N., and Weiner, D. B. (1995). The glucocorticoid receptor type II complex is a target of the HIV-1 vpr gene product. Proc. Natl. Acad. Sci. USA. 92:321-3625.

Levy, D. N., Refaeli, Y., and Weiner, D. B. (1995). Extracellular vpr protein increases cellular permissiveness to human immunodeficiency virus type 1 replication and reactivates virus from latency. J. Virol. 69:1243-1252.

Levy, D. N., Refaeli, Y., and Weiner, D. B. (1994). Serum vpr regulates productive infection and latency of human immunodeficiency virus type 1. Proc. Natl. Acad. Sci. USA. 91:10873-10877.

Levy, D. N., Fernandes, L. S., Williams, W. V., and Weiner, D. B. (1993). Induction of cell differentiation by human immunodeficiency virus 1 vpr. Cell. 72:541-550.

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 Book Chapters: 

Levy, D. N., Refaeli, Y., and Weiner, D. B. (1995). The vpr regulatory gene of HIV. In: Transacting functions of human retroviruses; Current Topics in Microbiology and Immunology. Vol 193. pp. 209-236. Springer-Verlag, Berlin. Chen, I.S.Y, Koprowski, H., Srinivasan, A, and Vogt. P.A., eds.

Levy, D. N. and Weiner, D. B. (1993). HIV-1 regulatory gene function analysis in a rhabdomyosarcoma cell line. pp. 243-249. Vaccines93, Modern Approaches to New Vaccines Including the Prevention of AIDS. Cold Spring Harbor Laboratory Press. Cold Spring Harbor, New York, N.Y.

Levy, D. N. and Weiner, D. B. (1993). Synthetic peptide-based vaccines and antiviral agents including HIV/AIDS as a model system. pp. 219-267. Biologically Active Peptides: Design, Synthesis, and Utilization. Williams, W.V. and Weiner, D.B., Eds. Technomic Publishing Company, Malvern, PA.