• The primary endpoint is viral load (HIV RNA) in plasma. [ Time Frame: at 12 and 24 weeks ] [ Designated as safety issue: No ]
  

• CD4 and CD8, absolute value, percentage and activation. [ Time Frame: during the 32 weeks of follow-up ] [ Designated as safety issue: No ]
  
• Total cholesterol, HDL and LDL in serum. [ Time Frame: during the 32 weeks of follow-up ] [ Designated as safety issue: Yes ]
  
• Cholesterol in cell membrane. [ Time Frame: during the 32 weeks of follow-up ] [ Designated as safety issue: Yes ]
  
• Symptoms reported by the patient following the interruption of the HAART therapy or signs detected by the clinician (classification according to the WHO), mainly those which may indicate acute antiretroviral symptoms. [ Time Frame: during the 32 weeks of follow-up ] [ Designated as safety issue: Yes ]
  
• Creatinine, urea, creatine kinase (CK), hepatic tests, (AST, ALT, GGT) [ Time Frame: during the 32 weeks of follow-up ] [ Designated as safety issue: Yes ]
  
• Proviral load. [ Time Frame: during the 32 weeks of follow-up ] [ Designated as safety issue: No ]
  

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.