Ignite Creation Date:
2025-12-24 @ 11:52 PM
Ignite Modification Date:
2025-12-25 @ 9:47 PM
Study NCT ID:
NCT00355251
Status:
TERMINATED
Last Update Posted:
2014-03-20
First Post:
2006-07-19
Is NOT Gene Therapy:
False
Has Adverse Events:
False
Brief Title:
Influence of Atorvastatin on Viral Replication During Antiretroviral Treatment Interruption
Sponsor:
Germans Trias i Pujol Hospital
Organization:
Study Overview
Official Title:
Study of the Influence of Atorvastatin in Plasma Viral Replication Given Prior to Antiretroviral Treatment Interruption in Patients With HIV-1 Infection and Viral Suppression.
Status:
TERMINATED
Status Verified Date:
2014-02
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
On the basis of published results of SMART study, it has been observed that the results are worse in patients who have interrupted their treatments.
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
To determine the influence of atorvastatin on plasma viral replication when the latter is given before and during highly active anti-retroviral therapy (HAART) in patients with HIV infection and viral suppression.
Detailed Description:
Recently, the inhibitory effect of the statins on the replication of the human immunodeficiency virus Type 1 (HIV-1) through two independent mechanisms of action has been described: the blockade of Rho guanosine triphosphatase that intervenes in the entry and exit of the virus and the blockade of the interaction between LFA-1 (leukocyte function antigen 1) and its ICAM 1 ligand (intercellular adhesion molecule 1) that intervenes in the process through which the virus binds to the target cell.
These initial data have led to the study of the effect of atorvastatin on the plasma replication of HIV in HIV+ patients that interrupt antiretroviral therapy (Ator Study 3) developed in our unit. The data of this study indicate that baseline plasma cholesterol determines viral load rebound on interrupting antiretroviral treatment. However, the introduction of atorvastatin on the day of interruption provided no virological or immunological benefit in comparison with an interruption of antiretrovirals without statins. This may be due to the fact that the potent inhibitory effect of atorvastatin is unable to compensate their activating effect on the production of HIV also described in our study.
Overall, our results pose a possible usefulness of atorvastatin in the control of viral replication if given before the interruption of antiretroviral therapy due to:
* Their capacity to reduce serum cholesterol at the time of interruption and consequently the cholesterol of the cell membrane.
* Their potent capacity to purge the HIV reservoir
Therefore, in this study we aim to investigate the impact of atorvastatin on viral replication when it is given 8 weeks before the interruption of the antiretroviral treatment and determine whether this impact is due to the reduction in serum and/or membrane cholesterol, or whether, on the other hand, there is a contribution by atorvastatin's capacity to induce the expression of viral products.
These initial data have led to the study of the effect of atorvastatin on the plasma replication of HIV in HIV+ patients that interrupt antiretroviral therapy (Ator Study 3) developed in our unit. The data of this study indicate that baseline plasma cholesterol determines viral load rebound on interrupting antiretroviral treatment. However, the introduction of atorvastatin on the day of interruption provided no virological or immunological benefit in comparison with an interruption of antiretrovirals without statins. This may be due to the fact that the potent inhibitory effect of atorvastatin is unable to compensate their activating effect on the production of HIV also described in our study.
Overall, our results pose a possible usefulness of atorvastatin in the control of viral replication if given before the interruption of antiretroviral therapy due to:
* Their capacity to reduce serum cholesterol at the time of interruption and consequently the cholesterol of the cell membrane.
* Their potent capacity to purge the HIV reservoir
Therefore, in this study we aim to investigate the impact of atorvastatin on viral replication when it is given 8 weeks before the interruption of the antiretroviral treatment and determine whether this impact is due to the reduction in serum and/or membrane cholesterol, or whether, on the other hand, there is a contribution by atorvastatin's capacity to induce the expression of viral products.
Study Oversight
Has Oversight DMC:
False
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
Secondary ID Infos
| Secondary ID | Type | Domain | Link | View |
|---|---|---|---|---|
| 2005-005356-41 | None | None | View |