Abstract

Studies of Acquired Immune Deficiency Syndrome (AIDS) are planned to focus on (a) laboratory research on the pathogenesis of AIDS and on specific anti-HTLV-III immunity in an epidemiologic context to delineate factors relevant to establishment of HTLV-III/LAV infection and to protection against the progrssion of HTLV-III/LAV infection to major immune cell damage and clinical AIDS; (b) clinical trials to treat or prevent HTLV-III/LAV infection, and the reultant opportunistic infections and to repair the immunologic deficiency in AIDs patients by use of anti-viral agents and cellular reconstitution and other means. Immunologic studies will focus on disorders within the CD4 populations, especially those occuring in the earliest periods after HTLV-III/LAV viral infections. Antibodies to HTLV-III/LAV that prevent immune cell damage and T cell and NK cell factors that help prevent KS and OI will be defined. Immune cell changes in the absence oif HTLV-III/LAV infection which may permit KS developmemt will be sought. A series of phase II trials are proposed for patients with AIDs-KS using several anti-HTLV-III drugs to determine their anti-retroviral and immunorestorative effects and whether eradication of the virus induces KS tumor regression. Also, anti-viral agents will be used prior to marrow infusion in order to facilitate immune restoration.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Project--Cooperative Agreements (U01)
Project #
5U01AI023606-03
Application #
3546624
Study Section
(SRC)
Project Start
1986-09-01
Project End
1991-08-31
Budget Start
1988-09-01
Budget End
1989-08-31
Support Year
3
Fiscal Year
1988
Total Cost
Indirect Cost

  Institution

Name
University of California Los Angeles
Department
Type
Schools of Medicine
DUNS #
119132785
City
Los Angeles
State
CA
Country
United States
Zip Code
90095

  Publications

Hofmann, B; Nishanian, P; Fan, J et al. (1994) HIV Gag p17 protein impairs proliferation of normal lymphocytes in vitro. AIDS 8:1016-7
Hofmann, B; Nishanian, P; Nguyen, T et al. (1993) Human immunodeficiency virus proteins induce the inhibitory cAMP/protein kinase A pathway in normal lymphocytes. Proc Natl Acad Sci U S A 90:6676-80
Hofmann, B; Bass, H; Nishanian, P et al. (1992) Different lymphoid cell populations produce varied levels of neopterin, beta 2-microglobulin and soluble IL-2 receptor when stimulated with IL-2, interferon-gamma or tumour necrosis factor-alpha. Clin Exp Immunol 88:548-54
Fahey, J L; Schooley, R (1992) Status of immune-based therapies in HIV infection and AIDS. Clin Exp Immunol 88:1-5
Popov, J; McGraw, T; Hofmann, B et al. (1992) Acute lymphoid changes and ongoing immune activation in SIV infection. J Acquir Immune Defic Syndr 5:391-9
Bass, H Z; Hardy, W D; Mitsuyasu, R T et al. (1992) Eleven lymphoid phenotypic markers in HIV infection: selective changes induced by zidovudine treatment. J Acquir Immune Defic Syndr 5:890-7
Bass, H Z; Hardy, W D; Mitsuyasu, R T et al. (1992) The effect of zidovudine treatment on serum neopterin and beta 2-microglobulin levels in mildly symptomatic, HIV type 1 seropositive individuals. J Acquir Immune Defic Syndr 5:215-21
Bass, H Z; Nishanian, P; Hardy, W D et al. (1992) Immune changes in HIV-1 infection: significant correlations and differences in serum markers and lymphoid phenotypic antigens. Clin Immunol Immunopathol 64:63-70
Hofmann, B; Nishanian, P; Fahey, J L et al. (1991) Serum increases and lymphoid cell surface losses of IL-2 receptor CD25 in HIV infection: distinctive parameters of HIV-induced change. Clin Immunol Immunopathol 61:212-24
Nishanian, P; Hofmann, B; Wang, Y et al. (1991) Serum soluble CD8 molecule is a marker of CD8 T-cell activation in HIV-1 disease. AIDS 5:805-12

Showing the most recent 10 out of 20 publications