Short-term Disulfiram Administration to Accelerate the Decay of the HIV Reservoir in Antiretroviral-treated HIV Infected Individuals
The purpose of this study is to determine whether a two-week course of disulfiram will reduce the HIV-1 latent reservoir in patients on highly active antiretroviral therapy (HAART).
|Study Design:||Endpoint Classification: Safety/Efficacy Study
Intervention Model: Single Group Assignment
Masking: Open Label
|Official Title:||Short-term Disulfiram Administration to Accelerate the Decay of the HIV Reservoir in Antiretroviral-treated HIV Infected Individuals|
- To determine if the addition of disulfiram to a stable antiretroviral regimen for two weeks results in decline in the size of the HIV-1 reservoir, as defined by the frequency of resting CD4+ T cells harboring replication competent HIV-1. [ Time Frame: 24 weeks ] [ Designated as safety issue: No ]
- To determine if the addition of disulfiram to a stable antiretroviral regimen for two weeks is associated with an immediate or transient increase in plasma HIV-1 RNA levels. [ Time Frame: Two weeks ] [ Designated as safety issue: Yes ]Real time viral load will be measured weekly during the treatment phase.
- To determine if the addition of disulfiram to a stable antiretroviral regimen for two weeks is safe and well tolerated. [ Time Frame: Two weeks ] [ Designated as safety issue: Yes ]
- To determine if the addition of disulfiram to a stable antiretroviral regimen for two weeks results in an increase in the frequency of activated CD4+ and CD8+ T cells in peripheral blood. [ Time Frame: 24 weeks ] [ Designated as safety issue: No ]
|Study Start Date:||January 2011|
|Study Completion Date:||May 2014|
|Primary Completion Date:||May 2014 (Final data collection date for primary outcome measure)|
|Experimental: Intervention Arm||
Open label 500mg disulfiram per day by mouth for 14 days
Other Name: Antabuse
This study is using a new approach to try and force HIV out of its protected cellular reservoirs.
Although current therapies are effective at "killing" new viruses that are produced, they are unable to access the virus in cells which were infected before antiretroviral therapy began. HIV can remain "hidden" in a latent (or resting) form in these cells for many years. Since these infected cells can live for many years, they are thought to be the most important barrier to HIV eradication (or "cure").
Many experts believe that one way to attack latent or "hidden" HIV is to use a drug than can "turn on" the virus and hence force HIV-1 out of resting T cells. In a recent study done in the laboratory, disulfiram proved to be among the most effective drugs currently available that can reactivate latent HIV-1,
Our primary hypothesis is that disulfiram will reduce the latent reservoir of HIV-1 in patients on highly active antiretroviral therapy (HAART). Theoretically, disulfiram will force HIV to replicate (grow) and thus result in the death of the infected cell. Standard antiretroviral drugs should prevent new cells from becoming infected. The end result of this process is that the total amount of HIV in the body will decline over time.
Please refer to this study by its ClinicalTrials.gov identifier: NCT01286259
|United States, California|
|San Francisco General Hospital|
|San Francisco, California, United States, 94110|
|United States, Maryland|
|Johns Hopkins University|
|Baltimore, Maryland, United States, 21205|
|Principal Investigator:||Steven G. Deeks, M.D.||University of California, San Francisco|
|Principal Investigator:||Adriana Andrade, M.D.||Johns Hopkins University|