Neurological complications are common in AIDS and with the expected increase in cases in the decade, the neurological disease must be of great concern. To devise appropriate strategies to prevent moderation and that of the AIDS dementia complex, we propose fundamental studies of pathogenesis. We will take advantage of our previous experience in a related lentivirus disease in sheep, visna, and our expertise with in situ hybridization technology to (1) define unambiguously the types of cells in AIDS dementia which harbor the causative agent (HIV); (2) evaluate the changes in the expression of macrophage genes such as IL-1 which might play a role in tissue damage; (3) differentially screen cDNA libraries to identify genes whose expression changes in concent with vacuolation, the most prominent pathological manifestation of the AIDS neurological disease.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Project (R01)
Project #
5R01AI025017-03
Application #
3138320
Study Section
(SSS)
Project Start
1987-07-01
Project End
1990-06-30
Budget Start
1989-07-01
Budget End
1990-06-30
Support Year
3
Fiscal Year
1989
Total Cost
Indirect Cost
Name
University of Minnesota Twin Cities
Department
Type
Schools of Medicine
DUNS #
168559177
City
Minneapolis
State
MN
Country
United States
Zip Code
55455
Cavert, W; Notermans, D W; Staskus, K et al. (1997) Kinetics of response in lymphoid tissues to antiretroviral therapy of HIV-1 infection. Science 276:960-4