***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Recent studies have shown that rosuvastatin significantly decreases serum levels of inflammatory biomarkers and slows progression of carotid atherosclerosis in the general population . However , there are no data about its effect on progression of atherosclerosis in HIV-infected patients . Adult patients with HIV infection , on stable antiretroviral therapy , with asymptomatic carotid atherosclerosis and hypercholesterolemia , who started a rosuvastatin treatment at 10 mg daily during the period 2007 - 2009 were enrolled and followed-up for 24 months . Thirty-six patients ( 30 males ) were enrolled , with a mean age of 49 years , a mean duration of current antiretroviral therapy of 38 months , and a mean 10-year risk of myocardial infa rct ion of 18.5 % .  Rosuvastatin led to a significant decrease in mean values of intima-media thickness in all extracranial carotid arteries , with the greatest magnitude observed in carotid bifurcations ( a mean decrease of 18.7 % in the right artery and of 21.4 % in the left artery ) and in internal carotid arteries ( a mean decrease of 23.7 % in the right artery and of 25.6 % in the left artery ) . Moreover , there was a significant reduction in mean levels of total cholesterol , low-density lipoprotein ( LDL ) cholesterol , and triglycerides versus respective baseline values associated with a significantly decreased mean cardiovascular risk . The treatment with rosuvastatin was well tolerated , and serious adverse events were not reported . A 24-month treatment with rosuvastatin in HIV-infected patients on highly active antiretroviral therapy ( HAART ) with sub clinical atherosclerosis and a moderate cardiovascular risk seems to promote significantly favorable changes in carotid atherosclerosis , associated with a favorable effect on serum lipid levels and a good tolerability profile BACKGROUND Lipoatrophy can complicate thymidine analogue nucleoside reverse transcriptase inhibitor (tNRTI)-based antiretroviral therapy ( ART ) . Lipoatrophy may be less likely with ART including ritonavir-boosted lopinavir ( LPV/r ) . Small , placebo-controlled studies found that uridine ( in tNRTI recipients ) and pravastatin improved HIV lipoatrophy over 12 weeks . Today , most patients with lipoatrophy receive non-tNRTI-based ART ; the effect of uridine in such patients is unknown . METHODS We performed a prospect i ve , r and omized trial in lipoatrophic adults with plasma HIV RNA<50 HIV-1 RNA copies/mL on tNRTI-sparing ART including LPV/r . Patients received uridine [ 36 g three times a day ( tid ) on 10 consecutive days per month ; n=10 ] , pravastatin [ 40 mg every night ( nocte ) ; n=12 ] , uridine plus pravastatin ( n=11 ) or neither ( n=12 ) for 24 weeks . The primary endpoint was mean change in limb fat mass as assessed by dual-energy X-ray absorptiometry ( DEXA ) . With 20 patients per intervention , the study had 80 % power to detect a mean difference between a treatment and the control of 0.5 kg , assuming a st and ard deviation of 0.9 and an alpha threshold equal to 5 % ( two-sided ) . RESULTS Of 45 participants ( all men , with median age 49.5 years and median limb fat 2.6 kg ) , two discontinued pravastatin and one participant stopped both pravastatin and uridine . The difference between the mean changes in limb fat mass for uridine vs. no uridine was 0.03 kg [ 95 % confidence interval ( CI ) -0.35 , + 0.28 ; P=0.79 ] . The respective difference for pravastatin was -0.03 kg ( 95 % CI -0.29 , + 0.34 ; P=0.84 ) . Pravastatin slightly decreased total cholesterol ( 0.44 mmol/L ; P=0.099 ) . Visceral adipose tissue measured by computed tomography did not change significantly . CONCLUSION In this population and at the doses used , neither uridine nor pravastatin for 24 weeks significantly increased limb fat mass OBJECTIVES To explore 48 week safety and efficacy of treatment simplification to atazanavir/ritonavir + lamivudine in HIV-infected patients with virological suppression on a stable atazanavir/ritonavir-based st and ard triple regimen . METHODS This was a single-arm pilot study , enrolling 40 patients on atazanavir/ritonavir + two nucleos(t)ide reverse transcriptase inhibitors ( NRTIs ) , without previous treatment failure , with HIV-RNA < 50 copies/mL for > 3 months and CD4 > 200 cells/mm(3 ) . At baseline , patients were switched to 300/100 mg of atazanavir/ritonavir + 300 mg of lamivudine once daily . Laboratory parameters , atazanavir plasma levels , self-reported adherence , quality of life , neurocognitive performance , bone composition and body fat distribution were monitored . Virological failure was defined as HIV-RNA > 50 copies/mL on two consecutive determinations or a single level > 1000 copies/mL. RESULTS After 48 weeks , 4/40 ( 10 % ) regimen discontinuations occurred : 1 death ( brain haemorrhage ) , 1 study withdrawal ( inadequate atazanavir plasma levels ) , 1 re-induction with two NRTIs due to pregnancy and 1 virological failure without development of resistance . Seven moderate to severe adverse events were recorded ( including four renal colics , possibly treatment-related ) in six patients . At week 48 , increases in total ( mean change + 17 mg/dL , P = 0.001 ) , high-density lipoprotein ( + 6 mg/dL , P < 0.001 ) and low-density lipoprotein ( + 8 mg/dL , P = 0.052 ) cholesterol were observed . The glomerular filtration rate improved ( + 7 mL/min/1.73 m(2 ) , P < 0.001 ) , as did scores exploring self-reported physical and mental health ( + 11 , P = 0.009 and + 13 , P < 0.001 on a 0 - 100 scale ) , neuropsychological performance ( -1 pathological task , P = 0.002 ) and total bone mineral density ( + 0.03 g/cm(2 ) , P = 0.026 ) . There were no significant changes in CD4 cell count , bilirubin , atazanavir plasma levels , adherence and body fat distribution over time . CONCLUSIONS Simplification to atazanavir/ritonavir + lamivudine was apparently safe and associated with rare virological failure , without resistance selection . This strategy deserves further investigation in a r and omized trial BACKGROUND HIV-infected patients have a high risk of  myocardial infa rct ion . We aim ed to assess the ability of statin treatment to reduce arterial inflammation and achieve regression of coronary atherosclerosis in this population . METHODS In a r and omised , double-blind , placebo-controlled trial , 40 HIV-infected participants with sub clinical coronary atherosclerosis , evidence of arterial inflammation in the aorta by fluorodeoxyglucose (FDG)-PET , and LDL-cholesterol concentration of less than 3.37 mmol/L ( 130 mg/dL ) were r and omly assigned ( 1:1 ) to 1 year of treatment with  atorvastatin or placebo . R and omisation was by the Massachusetts General Hospital ( MGH ) Clinical Research Pharmacy with a permuted-block algorithm , stratified by sex with a fixed block size of four . Study codes were available only to the MGH Research Pharmacy and not to study investigators or participants . The prespecified primary endpoint was arterial inflammation as assessed by FDG-PET of the aorta . Additional prespecified endpoints were non-calcified and calcified plaque measures and high risk plaque features assessed with coronary CT angiography and biochemical measures . Analysis was done by intention to treat with all available data and without imputation for missing data . The trial is registered with Clinical Trials.gov , number NCT00965185 . FINDINGS The study was done from Nov 13 , 2009 , to Jan 13 , 2014 . 19 patients were assigned to atorvastatin and 21 to placebo . 37 ( 93 % ) of 40 participants completed the study , with equivalent discontinuation rates in both groups . Baseline characteristics were similar between groups . After 12 months , change in FDG-PET uptake of the most diseased segment of the aorta was not different between atorvastatin and placebo , but technically adequate results comparing longitudinal changes in identical regions could be assessed in only 21 patients ( atorvastatin Δ -0.03 , 95 % CI -0.17 to 0.12 , vs placebo Δ -0.06 , -0.25 to 0.13 ; p=0.77 ) . Change in plaque could be assessed in all 37 people completing the study . Atorvastatin  reduced non-calcified coronary plaque volume relative to placebo : median change -19.4 % ( IQR -39.2 to 9.3 ) versus 20.4 % ( -7.1 to 94.4 ; p=0.009 , n=37 ) . The number of high-risk plaques was significantly reduced in the atorvastatin group compared with the placebo group : change in number of low attenuation plaques -0.2 ( 95 % CI -0.6 to 0.2 ) versus 0.4 ( 0.0 , 0.7 ; p=0.03 ; n=37 ) ; and change in number of positively remodelled plaques -0.2 ( -0.4 to 0.1 ) versus 0.4 ( -0.1 to 0.8 ; p=0.04 ; n=37 ) . Direct LDL-cholesterol ( -1.00 mmol/L , 95 % CI -1.38 to 0.61 vs 0.30 mmol/L , 0.04 to 0.55 , p<0.0001 ) and lipoprotein-associated phospholipase A2 ( -52.2 ng/mL , 95 % CI -70.4 to -34.0 , vs -13.3 ng/mL , -32.8 to 6.2 ; p=0.005 ; n=37 ) decreased significantly with atorvastatin relative to placebo . Statin therapy was well tolerated , with a low incidence of clinical adverse events . INTERPRETATION No significant effects of statin therapy on arterial inflammation of the aorta were seen as measured by FDG-PET . However , statin therapy reduced non-calcified plaque volume and high-risk coronary plaque features in HIV-infected patients . Further studies should assess whether reduction in high-risk coronary artery disease translates into effective prevention of cardiovascular events in this at-risk population . FUNDING National Institutes of Health , Harvard Clinical and Translational Science Center , National Center for Research Re sources OBJECTIVE T-cell activation independently predicts mortality , poor immune recovery and non-AIDS illnesses during combination antiretroviral therapy ( cART ) . Atorvastatin showed anti-immune activation effects among HIV-infected cART-naïve individuals . We investigated whether adjunct atorvastatin therapy reduces T-cell activation among cART-treated adults with suboptimal immune recovery . METHODS A r and omised double-blind placebo-controlled crossover trial , of atorvastatin 80 mg daily vs. placebo for 12 weeks , was conducted among individuals with CD4 increase < 295 cells/μl after seven years of suppressive cART .  Change in T-cell activation ( CD3 + CD4 + /CD8 + CD38 + HLADR+ ) and in T-cell exhaustion ( CD3 + CD4 + /CD8 + PD1 + ) was measured using flow cytometry . RESULTS Thirty patients were r and omised , 15 to each arm .  Atorvastatin result ed in a 28 % greater reduction in CD4 T-cell activation ( 60 % reduction ) than placebo ( 32 % reduction ) ; P = 0.001 . Atorvastatin also result ed in a 35 % greater reduction in CD8-T-cell activation  than placebo ( 49 % vs. 14 % , P = 0.0009 ) , CD4 T-cell exhaustion ( 27 % vs. 17 % in placebo ) , P = 0.001 and CD8 T-cell exhaustion ( 27 % vs. 16 % ) , P = 0.004 . There was no carry-over/period effect . Expected adverse events were comparable in both groups , and no serious adverse events were reported . CONCLUSION Atorvastatin  reduced T-cell immune activation and exhaustion among cART-treated adult 
    Output:
    
Meta-regression revealed that nucleoside reverse transcriptase inhibitors-sparing regimens were associated with reduced efficacy for statin 's ability to lower TC .
Statin therapy significantly lowers plasma TC and LDL levels in HIV-positive patients and is associated with low rates of adverse events .
Statins are effective and safe when dose-adjusted for drug-drug interactions with cART