Statins may play a role in preventing HIV disease progression
A recent study conducted by the National Naval Medical Center has demonstrated that statins, which are a class of drugs prescribed to lower cholesterol levels in people with high cholesterol, may benefit people living with HIV disease.
Previous studies have shown conflicting results on the antiviral activity of statins. In 2005, a study suggested that Mevacor (lovastatin), in addition to reducing cholesterol levels, may have the ability to reduce HIV replication. However, subsequent studies using Lipitor (atorvastatin), Zocor (simvastatin), and Pravachol (pravastatin) were not able to demonstrate the same results.
This new clinical trial evaluated the effects of Lipitor (atorvastatin) on HIV viral load and on markers of inflammation and immune activation. The trial included 24 HIV positive patients who were not on antiretroviral medication and who had high cholesterol levels that would benefit from statin treatment. The patients were not on antiretroviral medication during the trial, so that the researchers could observe the effect of Lipitor (at a high dose of 80 mg) on viral load compared to a placebo.
During eight weeks of Lipitor treatment, there were no overall changes in HIV replication compared to the placebo. The researchers did find reductions in inflammation and immune activation markers in the patients receiving Lipitor compared to those receiving the placebo. However, it is unclear whether these reductions are associated with slower disease progression or a reduced risk of complications.
Although the study did not demonstrate an overall ability of statins to suppress HIV replication, it did show that the short-term use of Lipitor resulted in decreased immune activation. Previous studies have emphasized the importance of immune activation in HIV disease progression and complications. Levels of inflammatory and immune activation markers correlate with disease progression in HIV-infected participants, and chronic persistent immune activation contributes to CD4 depletion.
The results of this recent trial warrant further investigation into the potential clinical benefits of statins for HIV infected patients. It is possible that statins may have an additive effect on viral replication when combined with antiretroviral therapy. Larger trials with longer durations of follow-up can help determine whether the reduction of inflammatory and immune activation markers from statin therapy will translate into less HIV disease progression.
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