Abstract

This application to develop a Center for AIDS Research at Duke University assembles the talents of over thirty independent investigators within six academic departments. All are engaged in AIDS or AIDS related research. Multiple disciplines are represented but the scientific programs are organized into four broad areas: (1) molecular mechanisms of host-HIV-1 interactions, (2) immunogenic epitopes of HIV proteins, (3) cellular responses to HIV-1 infection and (4) other human retroviruses and infectious agents in HIV-1 pathogenicity. The basic science programs interact closely with the clinical research program which includes both adult and pediatric components. Both basic and clinical research programs are fueled by seven core resources which provide support in (1) gene expression. (2) peptide synthesis, (3) retroviral biology, (4) flow cytometry, (5) Scid-Hu/transgenic mouse models, (6) data management and (7) procurement of human research material and protocol design. The remaining components represent plans for future growth and development, evaluation and administration.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Center Core Grants (P30)
Project #
5P30AI028662-02
Application #
3101100
Study Section
Special Emphasis Panel (SRC (28))
Project Start
1989-09-01
Project End
1994-06-30
Budget Start
1990-07-01
Budget End
1991-06-30
Support Year
2
Fiscal Year
1990
Total Cost
Indirect Cost

  Institution

Name
Duke University
Department
Type
Schools of Medicine
DUNS #
071723621
City
Durham
State
NC
Country
United States
Zip Code
27705

  Publications

Betts, Michael R; Exley, Barbara; Price, David A et al. (2005) Characterization of functional and phenotypic changes in anti-Gag vaccine-induced T cell responses and their role in protection after HIV-1 infection. Proc Natl Acad Sci U S A 102:4512-7
Ferrari, Guido; Neal, Wesley; Ottinger, Janet et al. (2004) Absence of immunodominant anti-Gag p17 (SL9) responses among Gag CTL-positive, HIV-uninfected vaccine recipients expressing the HLA-A*0201 allele. J Immunol 173:2126-33
Freel, Stephanie A; Fiscus, Susan A; Pilcher, Christopher D et al. (2003) Envelope diversity, coreceptor usage and syncytium-inducing phenotype of HIV-1 variants in saliva and blood during primary infection. AIDS 17:2025-33
Szczech, L A; Edwards, L J; Sanders, L L et al. (2002) Protease inhibitors are associated with a slowed progression of HIV-related renal diseases. Clin Nephrol 57:336-41
Bartlett, John A; Miralles, G Diego; Sevin, Anne D et al. (2002) Addition of cyclophosphamide to antiretroviral therapy does not diminish the cellular reservoir in HIV-infected persons. AIDS Res Hum Retroviruses 18:535-43
Szczech, Lynda Anne; Gange, Stephen J; van der Horst, Charles et al. (2002) Predictors of proteinuria and renal failure among women with HIV infection. Kidney Int 61:195-202
Wellons, M F; Ottinger, J S; Weinhold, K J et al. (2001) Immunologic profile of human immunodeficiency virus-infected patients during viral remission and relapse on antiretroviral therapy. J Infect Dis 183:1522-5
Demarest, J F; Jack, N; Cleghorn, F R et al. (2001) Immunologic and virologic analyses of an acutely HIV type 1-infected patient with extremely rapid disease progression. AIDS Res Hum Retroviruses 17:1333-44
Pilcher, C D; Shugars, D C; Fiscus, S A et al. (2001) HIV in body fluids during primary HIV infection: implications for pathogenesis, treatment and public health. AIDS 15:837-45
Johnston, A M; Valentine, M E; Ottinger, J et al. (2001) Immune reconstitution in human immunodeficiency virus-infected children receiving highly active antiretroviral therapy: a cohort study. Pediatr Infect Dis J 20:941-6

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