***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: BACKGROUND The short- and long-term effects of anti-hepatitis C treatment on mortality in the HIV-HCV-coinfected population have not been evaluated in observational cohorts . Such evaluations must use methods that allow for time-varying prognostic factors that both predict treatment and are affected by prior treatment . We aim ed to study immunological changes in HIV-HCV-coinfected individuals during HCV treatment  and to estimate the effect of  HCV-treatment  on mortality . METHODS Patients were included if they were aged ≥16 years , were HIV-HCV-coinfected and were enrolled in the COHERE cohort . Data were pooled within COHERE in December 2009 in EuroCoord . R and om-effects models were used to model immunological changes during HCV treatment . Marginal structural models were used to estimate the effect of  HCV  treatment on mortality , allowing for time-dependent confounders affected by prior treatment . RESULTS In total , 780/6,433 ( 12 % ) HIV-HCV-coinfected patients initiated HCV treatment ( interferon [ IFN ] and ribavirin n=692 , IFN alone n=88 ) . CD4(+ ) T-cell counts decreased during the first 12 weeks of treatment ( P<0.0001 ) and stabilized from week 24 onwards . The estimated mortality hazard ratio for comparing HCV-treated with -untreated individuals was 0.72 ( 95 % CI 0.43 , 1.21 ) . The estimated hazard ratio for liver-related death was 0.57 ( 95 % CI 0.21 , 1.55 ) . CONCLUSIONS Despite its effect in reducing CD4(+ ) T-cell counts , the effect of HCV treatment on mortality was in the direction of benefit and our results excluded a substantial increase in mortality . Such benefit may be related to a lower risk of liver-related death . New HCV treatment strategies might contribute to a further reduction in mortality Background Hepatitis C virus ( HCV ) is an RNA virus which has been known to cause acute and chronic necro-inflammatory disease of the liver . It is the leading cause of end-stage liver disease and hepatocellular carcinoma . HIV is known to have a negative impact on the natural disease outcome and immune response of HCV infection , whereas the reverse remains unclear . We evaluated the impact of HCV co-infection on recovery of CD4 + and CD8 + T-cells and liver enzyme levels before and after initiation of highly active antiretroviral therapy ( HAART ) in HIV/HCV co-infected patients . Methods A hospital-based , observational , prospect i ve cohort study design was used for this study .  Pre-antiretroviral treatment ( Pre-ART ) and under HAART HIV mono-infected and HCV/HIV co-infected individuals who are under regular follow-up were recruited for this study . 387 blood sample s were collected from volunteer , known HIV positive Ethiopian patients and screened for HCV . Twenty five HCV/HIV co-infected patients were prospect ively followed for four years . CD4 + and CD8 + T-cells and liver enzyme levels were determined annually for each of the participant . Results The prevalence of HCV/HIV co-infection in this study was 6.5 % . Both HCV/HIV co-infected and HIV mono-infected under HAART groups showed CD4 + recovery ( 343 Vs 426 ; P < 0.004 , OR = 4.97 , 95 % CI = 2.41 to 10.27 ) respectively ; but , the recovery rate was higher in mono-infected ( 80 Vs 426 ) than co-infected group ( 148 Vs 343 ) . The recovery and /or decline pattern of CD8 + T-cells was the same with that of CD4 + . In 75 % of co-infected groups , the mean alanine aminotransferase ( ALT ) and aspartate aminotransferase ( AST ) levels were above the upper limit of normal reference range . Analyses restricted to individuals who initiated HAART and pre-ART showed similar results . Conclusion We found that CD4 + T-cell recovery was negatively affected by the presence of ongoing HCV replication in under HAART co-infected individuals and fast decline of CD4 + T-cells in pre-ART patients . It was also associated with increased ALT and AST enzyme levels in both HAART initiated and treatment naïve co-infected patients Background The purpose of this study was to evaluate the efficacy and safety of three nevirapine-based antiretroviral treatments for adult antiretroviral-naïve Chinese patients with HIV-1 infection . Methodology This was a prospect i ve , multicenter study . 198 antiretroviral-naïve HIV-1 positive subjects with CD4 lymphocyte counts between 100/ul and 350/ul and plasma HIV-1 RNA levels more than 500 copies/ml were r and omized to start three NVP-based antiretroviral treatments : group A , NVP+AZT+ddI ; group B , NVP+3TC+d4 T ; group C , NVP+AZT+3TC .  Viral responses , immunologic responses , adverse events and drug resistence were monitored at baseline and the end of week 4 , 12 , 24 , 36 , 52 . Viralogical response and immunological response were also comparaed in different strata of baseline CD4 T lymphocyte counts and plasma HIV-1 RNA concentrations . At baseline , the plasma HIV-1 RNA was 4.44±0.68 , 4.52±0.71 and 4.41±0.63 lg copies/ml in group A , B and C respectively ( p = 0.628 ) . At the end of the study , the plasma viral load reached 2.54±1.11 , 1.89±0.46 and 1.92±0.58 lg copies/ml in group A , B and C respectively ( p<0.001 ) . At week 52 , suppression of plasma HIV-1 RNA to less than 50 copies/ml was achieved in more patients in group B and C than in group A ( 68.2 % , 69 % vs. 39.7 % ; p<0.001 ) . In planned subgroup analyses , the decrease of viral response rate was seen in group A when CD4 cell count > 200/ul ( subgroup H ) . But in subgroup L , viral response rate of three groups has no significant statistic difference . There were no statistically significant differences among three groups in immunological response wthin any of the CD4 or pVL strata . 3 out of 193 patients with available genotype at baseline showed primary drug resistant . Of 26 patients with virologic failure , 17 patients showed secondary drug resistant , 16 subjects in group A and 1 subject in group B. Logistic regression analysis indicated that presence of hepatotoxicity was associated with HCV-Ab positive ( OR = 2.096 , 95%CI : 1.106–3.973 , P = 0.023 ) and higher CD4 baseline ( CD4 count > 250/ul)(OR = 2.096 , 95%CI : 1.07–4.107 , P = 0.031 ) . Conclusion Our findings strongly support the use of 3TC+d4 T and 3TC+AZT as the nucleoside analogue combination in NVP-based antiretroviral therapy . The regimen of AZT+ddI+NVP produced poor virological response especially in the stratum of CD4 count more than 200/ul . More patients showed secondary drug resistant in this arm too . Patients with HCV-Ab+ and CD4 count > 250/ul appear to have significantly high risk of hepatoxicity . Trial Registration Clinical Trials.gov IMPORTANCE Patients co-infected with human immunodeficiency virus ( HIV ) and hepatitis C virus ( HCV ) are at high risk for liver disease progression . However , interferon-based treatments for HCV infection have significant toxicities , limiting treatment uptake . OBJECTIVE To assess the all-oral 3 direct-acting antiviral ( 3D ) regimen of ombitasvir , paritaprevir ( co-dosed with ritonavir [ paritaprevir/r ] ) , dasabuvir , and ribavirin in HCV genotype 1-infected adults with HIV-1 co-infection , including patients with cirrhosis . DESIGN , SETTING , AND PARTICIPANTS TURQUOISE-I is a r and omized , open-label study . Part 1a of this pilot study was conducted at 17 sites in the United States and Puerto Rico between September 2013 and August 2014 and included 63 patients with HCV genotype 1 and HIV-1 co-infection who were HCV treatment-naive or had history of prior treatment failure with peginterferon plus ribavirin therapy . The study allowed enrollment of patients , including those with cirrhosis , with a CD4 + count of 200/mm3 or greater or CD4 + percentage of 14 % or more and plasma HIV-1 RNA suppressed while taking a stable atazanavir- or raltegravir-inclusive antiretroviral regimen . INTERVENTIONS Ombitasvir/paritaprevir/r , dasabuvir , and ribavirin for 12 or 24 weeks of treatment as r and omized . MAIN OUTCOMES AND MEASURES The primary assessment was the proportion of patients with sustained virologic response ( HCV RNA < 25 IU/mL ) at posttreatment week 12 ( SVR12 ) . RESULTS Among patients receiving 12 or 24 weeks of 3D and ribavirin , SVR12 was achieved by 29 of 31 ( 94 % ; 95 % CI , 79%-98 % ) and 29 of 32 patients ( 91 % ; 95 % CI , 76%-97 % ) , respectively . Of the 5 patients who did not achieve SVR , 1 withdrew consent , 2 had confirmed virologic relapse or breakthrough , and 2 patients had clinical history and phylogenetic evidence consistent with HCV reinfection . The most common treatment-emergent adverse events were fatigue ( 48 % ) , insomnia ( 19 % ) , nausea ( 18 % ) , and headache ( 16 % ) . Adverse events were generally mild , with none reported as serious or leading to discontinuation . No patient had a confirmed HIV-1 breakthrough of 200 copies/mL or greater during treatment . CONCLUSIONS AND RELEVANCE In this open-label , r and omized uncontrolled study , treatment with the all-oral , interferon-free 3D-plus-ribavirin regimen result ed in high SVR rates among patients co-infected with HCV genotype 1 and HIV-1 whether treated for 12 or 24 weeks . Further phase 3 studies of this regimen are warranted in patients with co-infection . TRIAL REGISTRATION clinical trials.gov Identifier : NCT01939197 BACKGROUND Hepatitis C virus ( HCV ) infection is highly prevalent among HIV-1-infected individuals , but its contribution to the morbidity and mortality of coinfected patients who receive potent antiretroviral therapy  is controversial . We used data from the ongoing Swiss HIV Cohort Study to analyse clinical progression of HIV-1 , and the virological and immunological response to potent antiretroviral therapy  in HIV-1-infected patients with or without concurrent HCV infection . METHODS We analysed prospect i ve data on survival , clinical disease progression , suppression of HIV-1 replication , CD4-cell recovery , and frequency of changes in antiretroviral therapy according to HCV status in 3111 patients starting potent antiretroviral therapy .  RESULTS 1157 patients ( 37.2 % ) were coinfected with HCV , 1015 of whom ( 87.7 % ) had a history of intravenous drug use . In multivariate Cox 's regression , the probability of progression to a new AIDS-defining clinical event or to death was independently associated with HCV seropositivity ( hazard ratio 1.7 [ 95 % CI 1.26 - 2.30 ] ) , and with active intravenous drug use ( 1.38 [ 1.02 - 1.88 ] ) . Virological response to antiretroviral therapy  and the probability of treatment change were not associated with HCV serostatus . In contrast , HCV seropositivity was associated with a smaller CD4-cell recovery ( hazard ratio for a CD4-cell count increase of at least 50 cells/microL=0.79 [ 0.72 - 0.87 ] ) . INTERPRETATION HCV and active intravenous drug use could be important factors in the morbidity and mortality among HIV-1-infected patients , possibly through impaired CD4-cell recovery in HCV seropositive patients receiving potent antiretroviral therapy . These findings are relevant for decisions about optimum timing for HCV treatment in the setting of HIV infection IMPORTANCE There is an unmet need for interferon- and ribavirin-free treatment for chronic hepatitis C virus ( HCV ) infection in patients co-infected with human immunodeficiency virus ( HIV 
    Output:
    
A meta- analysis found no evidence of increased HIV VL associated with HCV co-infection or between HIV VL and HCV treatment with pegylated interferon-alpha-2a/b and ribavirin .
CONCLUSIONS This finding is in contrast to the substantial increases in HIV VL observed with several other systemic infections .