Office: (410) 955-9770
B.S. Campinas State University (Brazil), Biological Sciences
M.S. São Paulo State University (Brazil), Microbiology (Emphasis in Virology)
Ph.D. São Paulo State University (Brazil), Immunology
Lucio Gama started working at the Johns Hopkins School of Medicine as a molecular biologist under the supervision of Dr. Gerda Breitwieser in the Phisiology Department, studying the biological properties of the calcium receptor. Since 2001 he has been working as a laboratory manager for the Retrovirus Lab, and in 2006 he became a Research Associate, focusing his research on the innate immune aspects of SIV infection. In July 2011 he finished his Ph.D. in Immunology, under the mentorship of Dr. Esper Kallás at the University of São Paulo (USP), studying subpopulations of monocytes during HIV and SIV infection. He continues his research at Johns Hopkins, besides having an appointment as Visiting Scientist with the Department of Clinical Immunology at USP.
During his thesis project he characterized a new subset of immunosuppressive monocytes with a unique CD14+CD16-CCR2- classical phenotype. Currently he has identified similar subsets in other pathological conditions, and is now focusing in the biological events that lead to the rise of such populations. He is also evaluating restriction factors in monocytic cell lines with the goal of developing a monocyte/macrophage model for latency in SIV and HIV infection.
GAMA, L., SHIRK, E.N., RUSSELL, J.N., CARVALHO, K.I., LI, M., QUEEN, S.E., KALIL, J., ZINK, M.C., CLEMENTS, J.E., KALLAS, E.G. Expansion of a subset of CD14highCD16negCCR2low/neg monocytes functionally similar to myeloid-derived suppressor cells during SIV and HIV infection. J. Leukoc Bio. 2012 91(5):803-16.
ZARITSKY, L.A., GAMA, L., CLEMENTS, J.E. Canonical type I IFN signaling in Simian Immunodeficiency Virus-infected macrophages is disrupted by astrocyte-secreted CCL2. J Immunol. 2012 188(8):3876-85
CO J.G., WITWER, K.W., GAMA, L., ZINK, M.C., CLEMENTS, J.E. Induction of innate immune responses by SIV in vivo and in vitro: differential expression and function of RIG-I and MDA5. J. Infect Dis. 2011 204(7):1104-14.
QUEEN, S.E., MEARS, B.M., KELLY, K.M., DORSEY, J.L., LIAO, Z., DINOSO, J.B., GAMA, L., ADAMS, R.J., ZINK, M.C., CLEMENTS, J.E., KENT, S.J., MANKOWSKI, J.L. Replication-competent simian immunodeficiency virus (SIV) Gag escape mutations archived in latent reservoirs during antiretroviral treatment of SIC-infected macaques. J. Virol. 2011 85(17):9167-75.
ALAMMAR, L., GAMA, L., CLEMENTS, J.E. Simian immunodeficiency virus infection in the brain and lung leads to differential type I interferon signaling during acute infection J Immunol. 2011 186(7):4008-18.
CLEMENTS, J.E., GAMA, L., GRAHAM, D.R., MANKOWSKI, J.L., ZINK, M.C. A simian immunodeficiency virus macaque model of highly active retroviral treatment: viral latency in the periphery and the central nervous system. Curr Opin HIV AIDS. 2011 Jan; 6(1):37-42.
GRAHAM, D.R., GAMA, L., QUEEN, S.E., LI, M., BRICE, A.K., KELLY, K.M., MANKOWSKI, J.L., CLEMENTS, J.E. ZINK, M.C. Initiation of HAART during acute simian immunodeficiency virus infection rapidly controls virus replication in the CNS by enhancing immune activity and preserving protective immune responses. J Neurovirol. 2011 Feb;17(1):120-30.
Ravimohan, S., Gama, L., Barber, S.A., Clements, J.E. Regulation of SIV mac 239 basal long terminal repeat activity and viral replication in macrophages: functional roles of two CCAAT/enhancer-binding protein beta sites in activation and interferon beta-mediated suppression. class="apple-style-span" J Biol Chem. 2010 Jan 22;285(4):2258-73. Epub 2009 Nov 20.
Witwer, K.W., Gama, L., Li, M., Bartizal, C.M., Queen, S.E., Varrone, J.J., Brice, A.K., Graham, D.R., Tarwater, P.M., Mankowski, J.L., Zink, M.C., Clements, J.E. Coordinated regulation of SIV replication and immune responses in the CNS. class="apple-style-span" PLoS One. 2009 Dec 17;4(12):e8129.
Dinoso, J.B., Rabi, S.A., Blankson, J.N., Gama, L., Mankowski, J.L., Siliciano, R.F., Zink, M.C., Clements, J.E. A simian immunodeficiency virus-infected macaque model to study viral reservoirs that persist during highly active antiretroviral therapy. class="apple-style-span" J Virol. 2009 83(18):9247-57.