Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Project (R01)
Project #
3R01AI030350-05S1
Application #
2065555
Study Section
AIDS and Related Research Study Section 4 (ARRD)
Project Start
1990-06-01
Project End
1997-04-30
Budget Start
1995-05-01
Budget End
1996-04-30
Support Year
5
Fiscal Year
1995
Total Cost
Indirect Cost
Name
University of California San Francisco
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
073133571
City
San Francisco
State
CA
Country
United States
Zip Code
94143
Mackewicz, Carl E; Wang, Baikun; Metkar, Sunil et al. (2003) Lack of the CD8+ cell anti-HIV factor in CD8+ cell granules. Blood 102:180-3
Mackewicz, Carl E; Craik, Charles S; Levy, Jay A (2003) The CD8+ cell noncytotoxic anti-HIV response can be blocked by protease inhibitors. Proc Natl Acad Sci U S A 100:3433-8
Mackewicz, Carl E; Yuan, Jun; Tran, Patti et al. (2003) alpha-Defensins can have anti-HIV activity but are not CD8 cell anti-HIV factors. AIDS 17:F23-32
Levy, Jay A; Scott, Iain; Mackewicz, Carl (2003) Protection from HIV/AIDS: the importance of innate immunity. Clin Immunol 108:167-74
Levy, Jay A (2003) The search for the CD8+ cell anti-HIV factor (CAF). Trends Immunol 24:628-32
Mackewicz, C E; Lieberman, J; Froelich, C et al. (2000) HIV virions and HIV infection in vitro are unaffected by human granzymes A and B. AIDS Res Hum Retroviruses 16:367-72
Mackewicz, C E; Patterson, B K; Lee, S A et al. (2000) CD8(+) cell noncytotoxic anti-human immunodeficiency virus response inhibits expression of viral RNA but not reverse transcription or provirus integration. J Gen Virol 81:1261-4
Mackewicz, C E; Ridha, S; Levy, J A (2000) HIV virions and HIV replication are unaffected by granulysin. AIDS 14:328-30
Greco, G; Mackewicz, C; Levy, J A (1999) Sensitivity of human immunodeficiency virus infection to various alpha, beta and gamma chemokines. J Gen Virol 80 ( Pt 9):2369-73
Mackewicz, C E; Garovoy, M R; Levy, J A (1998) HLA compatibility requirements for CD8(+)-T-cell-mediated suppression of human immunodeficiency virus replication. J Virol 72:10165-70

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