Skip Navigation
Print This Page
Share this page: More

Lucio Gama, PhD

Assistant ProfessorLucio Gama
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 Physiology Department, studying the biological properties of the calcium sensing receptor. From 2001 to 2011 was the laboratory manager for the Retrovirus Lab under the mentorship of Dr. Clements and Dr. Zink. In 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 on 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. In the past two years, in collaboration with Dr. Amilcar Tanuri (University of Rio de Janeiro) and Dr. Luiz Pianowski (Kyolab Scientific), he has been evaluating a novel PKC activator, named ingenol-3-hexanoate, as a potential compound to be used for the reactivation of latent HIV and SIV in vivo.


  1. Gama, L., et al., Expansion of a subset of CD14highCD16negCCR2low/neg monocytes functionally similar to myeloid-derived suppressor cells during SIV and HIV infection. J Leukoc Biol, 2012. 91(5): p. 803-16.
  2. Ravimohan, S., et al., Early emergence and selection of a SIV-LTR C/EBP site variant in SIV-infected macaques that increases virus infectivity. PLoS One, 2012. 7(8): p. e42801.
  3. Zaritsky, L.A., L. Gama, and J.E. Clements, Canonical type I IFN signaling in simian immunodeficiency virus-infected macrophages is disrupted by astrocyte-secreted CCL2. J Immunol, 2012. 188(8): p. 3876-85.
  4. Metcalf Pate, K.A., et al., Platelet Activation and Platelet-Monocyte Aggregate Formation Contribute to Decreased Platelet Count During Acute Simian Immunodeficiency Virus Infection in Pig-tailed Macaques. J Infect Dis, 2013.
  5. Russell, J.N., J.E. Clements, and L. Gama, Quantitation of gene expression in formaldehyde-fixed and fluorescence-activated sorted cells. PLoS One, 2013. 8(9): p. e73849.
  6. Zaritsky, L.A., et al., Tissue-Specific Interferon Alpha Subtype Response to SIV Infection in Brain, Spleen, and Lung. J Interferon Cytokine Res, 2013. 33(1): p. 24-33.
  7. Abreu CM, Price SL, Shirk EN, Cunha RD, Pianowski LF, Clements JE, Tanuri A, Gama L (2014) Dual Role of Novel Ingenol Derivatives from Euphorbia tirucalli in HIV Replication: Inhibition of De Novo Infection and Activation of Viral LTR. PLoS ONE 9(5): e97257. 

© The Johns Hopkins University, The Johns Hopkins Hospital, and Johns Hopkins Health System. All rights reserved.

Privacy Policy and Disclaimer