Dr. Blankson is an infectious diseases fellow at the Johns Hopkins University and has spent the last three years working with his mentor, Dr. Robert Siliciano on HIV-1 latency and HIV-1 specific immunity. Through this award, Dr. Blankson hopes to conduct basic science research relating to these topics as a faculty member in infectious diseases at Johns Hopkins. He plans to characterize the latent virus isolates and HIV-1 specific immune responses of HIV-1 infected patients who spontaneously control viral replication. His hypothesis is that these patients form a heterogeneous group; some patients are infected with attenuated virus, others are infected with fully pathogenic virus but are able to control viral replication with vigorous HIV-1 specific immune responses. He plans to isolate latent virus from these patients and then to perform genotypic and phenotypic studies to assess the replication fitness of these isolates. He also plans to characterize their HIV-1 specific immune response with a special focus on identifying CD4+ and CD8+ T cell epitopes. The sequence of autologous latent virus at these epitopes will be analyzed for evidence of selective pressure exerted by the immune system. Dr. Blankson will attend basic immunology and virology seminars as well as clinical medicine and infectious diseases conferences. This along with the excellent mentorship of Dr. Siliciano, and the supportive environment of the Johns Hopkins University will provide Dr. Blankson with the skills he needs to develop into an independent clinician and basic scientist researcher in HIV-1 pathogenesis.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Clinical Investigator Award (CIA) (K08)
Project #
5K08AI051191-02
Application #
6617853
Study Section
Acquired Immunodeficiency Syndrome Research Review Committee (AIDS)
Program Officer
Young, Janet M
Project Start
2002-08-01
Project End
2007-07-31
Budget Start
2003-08-01
Budget End
2004-07-31
Support Year
2
Fiscal Year
2003
Total Cost
$115,290
Indirect Cost
Name
Johns Hopkins University
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
001910777
City
Baltimore
State
MD
Country
United States
Zip Code
21218
Han, Yefei; Lai, Jun; Barditch-Crovo, Patricia et al. (2008) The role of protective HCP5 and HLA-C associated polymorphisms in the control of HIV-1 replication in a subset of elite suppressors. AIDS 22:541-4
Bailey, Justin R; O'Connell, Karen; Yang, Hung-Chih et al. (2008) Transmission of human immunodeficiency virus type 1 from a patient who developed AIDS to an elite suppressor. J Virol 82:7395-410
Chase, Amanda J; Yang, Hung-Chih; Zhang, Hao et al. (2008) Preservation of FoxP3+ regulatory T cells in the peripheral blood of human immunodeficiency virus type 1-infected elite suppressors correlates with low CD4+ T-cell activation. J Virol 82:8307-15
Dinoso, Jason B; Kim, Scott Y; Siliciano, Robert F et al. (2008) A comparison of viral loads between HIV-1-infected elite suppressors and individuals who receive suppressive highly active antiretroviral therapy. Clin Infect Dis 47:102-4
Andrade, Adriana; Bailey, Justin R; Xu, Jie et al. (2008) CD4+ T cell depletion in an untreated HIV type 1-infected human leukocyte antigen-B*5801-positive patient with an undetectable viral load. Clin Infect Dis 46:e78-82
Gandhi, Shiv K; Siliciano, Janet D; Bailey, Justin R et al. (2008) Role of APOBEC3G/F-mediated hypermutation in the control of human immunodeficiency virus type 1 in elite suppressors. J Virol 82:3125-30
Bailey, Justin R; Zhang, Haili; Wegweiser, Barbara W et al. (2007) Evolution of HIV-1 in an HLA-B*57-positive patient during virologic escape. J Infect Dis 196:50-5
Blankson, Joel N; Bailey, Justin R; Thayil, Seema et al. (2007) Isolation and characterization of replication-competent human immunodeficiency virus type 1 from a subset of elite suppressors. J Virol 81:2508-18
Bailey, Justin R; Williams, Thomas M; Siliciano, Robert F et al. (2006) Maintenance of viral suppression in HIV-1-infected HLA-B*57+ elite suppressors despite CTL escape mutations. J Exp Med 203:1357-69