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Lucio Gama, PhD

Lucio Gama

Assistant Professor
Email: lucio@jhmi.edu
Office: (410) 955-9770

Education:

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

Bio:

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.

Publications:

  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.
 
 
 
 
 

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