Statins may help fight HIV - Scientists have found that statins may slow down the progression of HIV infection. In a recent multicenter clinical trial of atorvastatin, a type of cholesterol-lowering drug, the researchers found that although the drug did not inhibit plasma HIV RNA levels, it did inhibit expression of cellular markers of immune activation and inflammation in patients with HIV infection.
Since immune activation and inflammation are associated with progression of HIV infection, the implication is that the statin may inhibit disease progression and help in the infection’s management.
The study, led by Anuradha Ganesan, at the Uniformed Services University of the Health Sciences in Bethesda, Md., randomized 22 HIV-1-infected patients not on antiretroviral therapy and with cholesterol levels lower than those requiring statin therapy in a double-blind protocol of high-dose drug or placebo for eight weeks.
After a four-to-six-week washout phase, each group was switched to the other treatment for another eight weeks. The primary objective was to study the effect of atorvastatin on plasma HIV-1 RNA levels, as previous studies had shown conflicting results.
The effect on cellular markers of immune activation was a secondary objective. HIV-1 RNA levels were not significantly affected by the drug, but levels of such immune activation markers as CD38 and HLA-DR on CD4 and CD8 T cells were reduced. The researchers noted that their findings with atorvastatin suggest that understanding the mechanism by which statins affect immune markers may identify new approaches for the management of HIV infection. The study was published in The Journal of Infectious Diseases. Washington: (ANI)
Since immune activation and inflammation are associated with progression of HIV infection, the implication is that the statin may inhibit disease progression and help in the infection’s management.
The study, led by Anuradha Ganesan, at the Uniformed Services University of the Health Sciences in Bethesda, Md., randomized 22 HIV-1-infected patients not on antiretroviral therapy and with cholesterol levels lower than those requiring statin therapy in a double-blind protocol of high-dose drug or placebo for eight weeks.
After a four-to-six-week washout phase, each group was switched to the other treatment for another eight weeks. The primary objective was to study the effect of atorvastatin on plasma HIV-1 RNA levels, as previous studies had shown conflicting results.
The effect on cellular markers of immune activation was a secondary objective. HIV-1 RNA levels were not significantly affected by the drug, but levels of such immune activation markers as CD38 and HLA-DR on CD4 and CD8 T cells were reduced. The researchers noted that their findings with atorvastatin suggest that understanding the mechanism by which statins affect immune markers may identify new approaches for the management of HIV infection. The study was published in The Journal of Infectious Diseases. Washington: (ANI)
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