The mission of the UAB CFAR is to stimulate and support multidisciplinary basic, behavioral, clinical and translational AIDS research so as to hasten the development of effective treatments and prevention strategies for AIDS. For 20 years, the Center has played a vital role in supporting cutting edge research activities of its members that have led to paradigm-shifting discoveries, including: the discovery of HIV-1 quasispecies diversity (Nature 1988), detection of HIV-1 RNA in plasma (Science 1993), viral dynamics in acute and chronic infection (NEJM 1991;Nature 1995), HIV-1 escape from cytotoxic T-cells (Nat Medicine 1997) and neutralizing antibodies (Nature 2003), first-in-human phase 1 clinical studies of 7 currently approved therapies (NEJM 1993;Nat Medicine 1998;JAMA 2006), the zoonotic origins of HIV-1 (Nature 1999;Nature 2006;Science 2006), and the identification of the transmitted HIV-1 envelope and complete genome/proteome responsible for HIV infection (PNAS 2008). A common thread connecting all of these discoveries is the proactive participation of the CFAR in facilitating basic, translational and clinical research through effective collaboration between basic and clinical investigators. The objectives of the CFAR reflect this continuing commitment to innovative, multidisciplinary AIDS research and include: 1. To provide a central institutional focus for HIV/AIDS research activities that emphasize effective communication and collaboration among CFAR members and the wider HIV/AIDS research community. 2. To enhance productivity of ongoing research programs by encouraging interdisciplinary research and by providing critical shared resource facilities and administrative and fiscal management support to Center investigators. 3. To use robust strategic planning methods to identify new research opportunities and priorities, to align them with existing CFAR programs, and to foster new research programs where none are in existence but where faculty interest and University capacity is evident. 4. To stimulate the entry of junior and established faculty into HIV/AIDS research programs. This is accomplished through mentoring young investigators and by a peer-reviewed Developmental Grants Program. 5. To stimulate faculty recruitment and program development in areas that reflect the ongoing evolution of HIV/AIDS research and the global epidemic. The Center is comprised of 163 Center members from 35 Divisions and Departments within UAB funded by current AIDS-related grants and contracts totaling more than $87.2 million. Nine Core Facilities are proposed that provide vital support for the Center's principal thematic areas of viral pathogenesis, experimental therapeutics, global health, prevention and vaccine development. The success of the UAB CFAR in stimulating HIV/AIDS research is reflected in the growth in NIH extramural funding for AIDS-related research from $6.0 million in NIH funding in 1988 to over $26 million currently, in over 2500 research publications over the past six year grant period, in the recruitment of more than 21 HIV/AIDS investigators since 2QQ2, and in the garnering of strong Institutional support.

Public Health Relevance

The UAB CFAR will stimulate and facilitate HIV/AIDS research that has high national and international impact and in so doing will promote the NIH priorities of innovation and effectiveness iin AIDS research, treatment and prevention.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Center Core Grants (P30)
Project #
5P30AI027767-24
Application #
8306299
Study Section
Special Emphasis Panel (ZAI1-SV-A (J3))
Program Officer
Namkung, Ann S
Project Start
1997-03-01
Project End
2014-05-31
Budget Start
2012-06-01
Budget End
2013-05-31
Support Year
24
Fiscal Year
2012
Total Cost
$4,882,714
Indirect Cost
$1,520,083
Name
University of Alabama Birmingham
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
063690705
City
Birmingham
State
AL
Country
United States
Zip Code
35294
Bateman, Allen C; Chibwesha, Carla J; Parham, Groesbeck P (2015) Minimizing verification bias in cervical cancer screening of HIV-infected women. Int J Gynaecol Obstet 128:269-70
Miller, Michelle M; Akaronu, Nnenna; Thompson, Elizabeth M et al. (2015) Modulating DNA methylation in activated CD8+ T cells inhibits regulatory T cell-induced binding of Foxp3 to the CD8+ T Cell IL-2 promoter. J Immunol 194:990-8
Li, Jun; Hsu, Hui-Chen; Ding, Yana et al. (2014) Inhibition of fucosylation reshapes inflammatory macrophages and suppresses type II collagen-induced arthritis. Arthritis Rheumatol 66:2368-79
Mugavero, Michael J; Westfall, Andrew O; Cole, Stephen R et al. (2014) Beyond core indicators of retention in HIV care: missed clinic visits are independently associated with all-cause mortality. Clin Infect Dis 59:1471-9
Stevenson, Catherine; de la Rosa, Gonzalo; Anderson, Christopher S et al. (2014) Essential role of Elmo1 in Dock2-dependent lymphocyte migration. J Immunol 192:6062-70
Yuan, Furong; Yosef, Nejla; Lakshmana Reddy, Chetan et al. (2014) CCR2 gene deletion and pharmacologic blockade ameliorate a severe murine experimental autoimmune neuritis model of Guillain-Barré syndrome. PLoS One 9:e90463
Parker, Ivana Kennedy; Roberts, Ladeidra Monet; Hansen, Laura et al. (2014) Pro-atherogenic shear stress and HIV proteins synergistically upregulate cathepsin K in endothelial cells. Ann Biomed Eng 42:1185-94
Huijbregts, Richard P H; Michel, Katherine G; Hel, Zdenek (2014) Effect of progestins on immunity: medroxyprogesterone but not norethisterone or levonorgestrel suppresses the function of T cells and pDCs. Contraception 90:123-9
Sarzotti-Kelsoe, Marcella; Daniell, Xiaoju; Todd, Christopher A et al. (2014) Optimization and validation of a neutralizing antibody assay for HIV-1 in A3R5 cells. J Immunol Methods 409:147-60
Li, Hao; Hsu, Hui-Chen; Wu, Qi et al. (2014) IL-23 promotes TCR-mediated negative selection of thymocytes through the upregulation of IL-23 receptor and ROR?t. Nat Commun 5:4259

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