Immunologic Control of Drug Resistant HIV
Recruitment status was Active, not recruiting
Drug resistant HIV strains often develop in patients who have taken anti-HIV drugs for an extended time. However, these drug resistant HIV strains do not always cause an increase in the level of HIV in the blood. This study will explore why some patients with drug resistant virus continue to have low viral loads.
|Study Design:||Observational Model: Cohort
Time Perspective: Prospective
|Official Title:||Observational Study of HIV Infected Adults With Detectable Plasma HIV-1 RNA Levels Between 200 and 10,000 Copies/mL While Receiving Stable Antiretroviral Therapy|
|Study Start Date:||March 2003|
|Estimated Study Completion Date:||December 2008|
|Primary Completion Date:||December 2006 (Final data collection date for primary outcome measure)|
Despite the emergence of high level drug resistance in HIV-infected patients on stable antiretroviral therapy, plasma HIV RNA levels generally remain below the pretherapy viral load "set-point". The virologic and immunologic determinants of this lower steady state level of viremia have not been defined. Preliminary data indicate that: 1) drug resistant variants have reduced replicative capacity and pathogenic potential; 2) drug resistant viremia is associated with reduced T cell activation and turnover compared to wild-type viremia; and 3) patients with low level drug resistant viremia often have HIV-specific CD4 cells that are absent in patients with higher levels of viremia. This study will investigate whether the emergence of a poorly fit, drug resistant variant results in the generation of an effective HIV-specific CD4 cell response and if this response contributes to the establishment of a lower steady state level of viremia.
Participants in this study will be followed for 2 years or until antiretroviral therapy is modified or discontinued. Study visits will occur every 2 months, for a total of 14 visits. Study visits will include a patient interview and blood tests to measure the breadth and magnitude of the HIV-specific CD4 and CD8 cell responses as a function of viral load, viral replicative capacity, drug resistance phenotype, T cell turnover, and thymic function.
|United States, California|
|San Francisco General Hospital|
|San Francisco, California, United States, 94110|
|Study Chair:||Steven G. Deeks, MD||Department of Medicine, University of California - San Francisco|