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Joel N. Blankson, MD, PhD

Department Affiliations Department of Infectious Diseases, Molecular and Comparative Pathobiology
Rank Associate Professor
Office Phone 410-955-7757
Lab Phone
Fax 443-287-6218
Email jblanks@jhmi.edu
SOM Address 552 Rangos
Website
Students

Abena Kwaa 2015

Research Interests

Our laboratory focuses on understanding the mechanisms of control of viral replication in rare HIV-1 infected patients who maintain undetectable viral loads in the absence of antiretroviral therapy. We are studying viral and host factors in these patients with the hope of being to apply the principles to a therapeutic vaccine. We have shown that CD8+ T cells are effective at suppressing viral replication in vitro and we are studying the exact mechanisms of control. We are also trying to determine whether natural killer cells play a role in some instances and whether effector cells are capable of controlling viral replication in macrophages as well as in CD4+ T cells

Publications

  • Buckheit RW 3rd, Siliciano RF, Blankson JN. Primary CD8+ T cells from elite suppressors effectively eliminate non-productively HIV-1 infected resting and activated CD4+ T cells. Retrovirology. 2013
  • Buckheit RW 3rd, Salgado M, Silciano RF, Blankson JN. Inhibitory potential of subpopulations of CD8+ T cells in HIV-1-infected elite suppressors. J Virol. 2012;86:13679-88.
  • Buckheit RW 3rd, Allen TG, Alme A, Salgado M, O’Connell KA, Huculak S, Falade-Nwulia O, Williams TM, Gallant JE, Siliciano RF, Blankson JN. Host factors dictate control of viral replication in two HIV-1 controller/chronic progressor transmission pairs. Nat Commun. 2012 6;3:716.
  • Salgado M, Rabi SA, O’Connell KA, Buckheit RW 3rd, Bailey JR, Chaudhry AA, Breaud AR, Marzinke MA, Clarke W, Margolick JB, Siliciano RF, Blankson JN. Prolonged control of replication-competent dual- tropic human immunodeficiency virus-1 following cessation of highly active antiretroviral therapy. Retrovirology. 2011 5;8:97
  • O’Connell KA, Rabi SA, Siliciano RF, Blankson JN. CD4+ T cells from elite suppressors are more susceptible to HIV-1 but produce fewer virions than cells from chronic progressors. Proc Natl Acad Sci U S A. 2011;108 :E689-98.