Background Mortality among HIV-infected persons is decreasing, and causes of death are changing. Classification of deaths is hampered because of low autopsy rates, frequent deaths outside of hospitals, and shortcomings of International Statistical Classification of Diseases and Related Health Problems (ICD-10) coding. Methods We studied mortality among Swiss HIV Cohort Study (SHCS) participants (19882010) and causes of death using the Coding Causes of Death in HIV (CoDe) protocol (20052009). Furthermore, we linked the SHCS data to the Swiss National Cohort (SNC) cause of death registry. Results AIDS-related mortality peaked in 1992 [11.0/100 person-years (PY)] and decreased to 0.144/100 PY (2006); non-AIDS-related mortality ranged between 1.74 (1993) and 0.776/100 PY (2006); mortality of unknown cause ranged between 2.33 and 0.206/100 PY. From 2005 to 2009, 459 of 9053 participants (5.1%) died. Underlying causes of deaths were: non-AIDS malignancies [total, 85 (19%) of 446 deceased persons with known hepatitis C virus (HCV) status; HCV-negative persons, 59 (24%); HCV-coinfected persons, 26 (13%)]; AIDS [73 (16%); 50 (21%); 23 (11%)]; liver failure [67 (15%); 12 (5%); 55 (27%)]; non-AIDS infections [42 (9%); 13 (5%); 29 (14%)]; substance use [31 (7%); 9 (4%); 22 (11%)]; suicide [28 (6%); 17 (7%), 11 (6%)]; myocardial infarction [28 (6%); 24 (10%), 4 (2%)]. Characteristics of deceased persons differed in 2005 vs. 2009: median age (45 vs. 49 years, respectively); median CD4 count (257 vs. 321 cells/L, respectively); the percentage of individuals who were antiretroviral therapy-naive (13 vs. 5%, respectively); the percentage of deaths that were AIDS-related (23 vs. 9%, respectively); and the percentage of deaths from non-AIDS-related malignancies (13 vs. 24%, respectively). Concordance in the classification of deaths was 72% between CoDe and ICD-10 coding in the SHCS; and 60% between the SHCS and the SNC registry. Conclusions Mortality in HIV-positive persons decreased to 1.33/100 PY in 2010. Hepatitis B or C virus coinfections increased the risk of death. Between 2005 and 2009, 84% of deaths were non-AIDS-related. Causes of deaths varied according to data source and coding system.
Objectives The aim of this study was to estimate the relative risk of cardiovascular disease (CVD) among people living with HIV (PLHIV) compared with the HIV-uninfected population. Methods We conducted a systematic review and meta-analysis of studies from the peer-reviewed literature. We searched the Medline database for relevant journal articles published before August 2010. Eligible studies were observational and randomized controlled trials, reporting CVD, defined as myocardial infarction (MI), ischaemic heart disease, cardiovascular and cerebrovascular events or coronary heart disease among HIV-positive adults. Pooled relative risks were calculated for various groupings, including different classes of antiretroviral therapy (ART). Results The relative risk of CVD was 1.61 [95% confidence interval (CI) 1.431.81] among PLHIV without ART compared with HIV-uninfected people. The relative risk of CVD was 2.00 (95% CI 1.702.37) among PLHIV on ART compared with HIV-uninfected people and 1.52 (95% CI 1.351.70) compared with treatment-naive PLHIV. We estimate the relative risk of CVD associated with protease inhibitor (PI)-, nucleoside reverse transcriptase inhibitor- and nonnucleoside reverse transcriptase inhibitor-based ART to be 1.11 (95% CI 1.051.17), 1.05 (95% CI 1.011.10) and 1.04 (95% CI 0.991.09) per year of exposure, respectively. Not all ART was associated with increased risk; specifically, lopinavir/ritonavir and abacavir were associated with the greater risk and the relative risk of MI for PI-based versus non-PI-based ART was 1.41 (95% CI 1.201.65). Conclusion PLHIV are at increased risk of cardiovascular disease. Although effective in prolonging survival, ART (in particular PI-based regimens) is related to further increased risk of CVD events among people at highest initial absolute risk of cardiovascular disease.
ObjectivesDolutegravir (DTG), a second-generation integrase strand transfer inhibitor (INSTI), is now among the most frequently used antiretroviral agents. However, recent reports have raised concerns about potential neurotoxicity. MethodsWe performed a retrospective analysis of a cohort of HIV-infected patients who had initiated an INSTI in two large German out-patient clinics between 2007 and 2016. We compared discontinuation rates because of adverse events (AEs) within 2 years of starting treatment with dolutegravir, raltegravir or elvitegravir/cobicistat. We also evaluated factors associated with dolutegravir discontinuation. ResultsA total of 1950 INSTI-based therapies were initiated in 1704 patients eligible for analysis within the observation period. The estimated rates of any AE and of neuropsychiatric AEs leading to discontinuation within 12 months were 7.6% and 5.6%, respectively, for dolutegravir (n = 985), 7.6% and 0.7%, respectively, for elvitegravir (n = 287), and 3.3% and 1.9%, respectively, for raltegravir (n = 678). Neuropsychiatric AEs leading to dolutegravir discontinuation were observed more frequently in women [hazard ratio (HR) 2.64; 95% confidence interval (CI) 1.23-5.65; P = 0.012], in patients older than 60 years (HR: 2.86; 95% CI: 1.42-5.77; P = 0.003) and in human leucocyte antigen (HLA)-B*5701-negative patients who initiated abacavir at the same time (HR: 2.42; 95% CI: 1.38-4.24; P = 0.002). ConclusionsIn this large cohort, the rate of discontinuation of dolutegravir because of neuropsychiatric adverse events was significantly higher than for other INSTIs, at almost 6% within 12 months. Despite the limitations of this retrospective study, the almost three-fold higher discontinuation rates observed amongst women and older patients underscore the need for further investigation, especially in patient populations usually underrepresented in clinical trials.
Objectives Across Europe, almost a third of individuals infected with HIV do not enter health care until late in the course of their infection. Surveillance to identify the extent to which late presentation occurs remains inadequate across Europe and is further complicated by the lack of a common clinical definition of late presentation. The objective of this article is to present a consensus definition of late presentation of HIV infection. Methods Over the past year, two initiatives have moved towards a harmonized definition. In spring 2009, they joined efforts to identify a common definition of what is meant by a 'late-presenting' patient. Results Two definitions were agreed upon, as follows. Late presentation: persons presenting for care with a CD4 count below 350 cells/mu L or presenting with an AIDS-defining event, regardless of the CD4 cell count. Presentation with advanced HIV disease: persons presenting for care with a CD4 count below 200 cells/mL or presenting with an AIDS-defining event, regardless of the CD4 cell count. Conclusion The European Late Presenter Consensus working group believe it would be beneficial if all national health agencies, institutions, and researchers were able to implement this definition ( either on its own or alongside their own preferred definition) when reporting surveillance or research data relating to late presentation of HIV infection.
The overall purpose of these guidelines is to provide guidance on best clinical practice in the treatment and management of adults with HIV infection with antiretroviral therapy (ART). The scope includes: (i) guidance on the initiation of ART in those previously naïve to therapy; (ii)support of patients on treatment; (iii) management of patients experiencing virological failure; and (iv) recommendations in specific patient populations where other factors need to be taken into consideration. The guidelines are aimed at clinical professionals directly involved with and responsible for the care of adults with HIV infection and at community advocates responsible for promoting the best interests and care of HIV-positive adults. They should be read in conjunction with other published BHIVA guidelines.
Objective This paper presents the final analysis of once-daily darunavir/ritonavir (DRV/r) vs. lopinavir/ritonavir (LPV/r) in treatment-naive HIV-1-infected adults. Methods Subjects; NCT00258557) was a randomized, open-label, phase-III, 192-week trial. Patients were stratified by baseline HIV-1 RNA and CD4 count, and randomized to once-daily DRV/r 800/100?mg or LPV/r 800/200?mg total daily dose (either once or twice daily) plus tenofovir/emtricitabine. Results Of 689 randomized patients receiving treatment (DRV/r: 343; LPV/r: 346), 85 and 114 patients in the DRV/r and LPV/r arms, respectively, had discontinued by week 192. Noninferiority was shown in the primary endpoint of virological response (HIV-1 RNA?50 copies/mL) [DRV/r: 68.8%; LPV/r: 57.2%; P?0.001; intent to treat (ITT)/time to loss of virological response; estimated difference in response 11.6% (95% confidence interval 4.418.8%)]. Statistical superiority in virological response of DRV/r over LPV/r was demonstrated for the primary endpoint (P?=?0.002) and for the ITT non-virological-failure-censored analysis (87.4% vs. 80.8%, respectively; P?=?0.040). No protease inhibitor (PI) primary mutations developed and only low levels of nucleoside reverse transcriptase inhibitor (NRTI) resistance developed in virological failures in both groups. Significantly fewer discontinuations because of adverse events were observed with DRV/r (4.7%) than with LPV/r (12.7%; P?=?0.005). Grade 24 treatment-related diarrhoea was significantly less frequent with DRV/r than with LPV/r (5.0% vs. 11.3%, respectively; P?=?0.003). DRV/r was associated with smaller median increases in total cholesterol and triglyceride levels than LPV/r. Changes in low- and high-density lipoprotein cholesterol were similar between groups. Similar increases in aspartate aminotransferase and alanine aminotransferase for DRV/r and LPV/r were observed. Conclusion Over 192 weeks, once-daily DRV/r was noninferior and statistically superior in virological response to LPV/r, with a more favourable gastrointestinal profile, demonstrating its suitability for long-term use in treatment-naive patients.
1.Levels of evidence1.1Reference2.Introduction3.Auditable targets4.Table summaries4.1Initial diagnosis4.2Assessment of ART-naive individuals4.3ART initiation4.4Initial assessment following commencement of ART4.5Routine monitoring on ART4.6References5.Newly diagnosed and transferring HIV-positive individuals5.1Initial HIV-1 diagnosis5.2Tests to determine whether acquisition of HIV infection is recent5.3Individuals transferring care from a different HIV healthcare setting5.4Communication with general practitioners and shared care5.5Recommendations5.6References6.Patient history6.1Initial HIV-1 diagnosis6.2Monitoring of ART-naive patients6.3Pre-ART initiation assessment6.4Monitoring individuals established on ART6.5Assessment of adherence6.6Recommendations6.7References7.Exam ination7.1Recommendations8.Identifying the need for psychological support8.1References9.Assessment of immune status9.1CD4 T cell counts9.2CD4 T cell percentage9.3References10.HIV viral load10.1Initial diagnosis/ART naive10.2Post ART initiation10.3Individuals established on ART10.4Recommendations10.5References11.Technic al aspects of viral load testing11.1References12.Viral load kinetics during ART and viral load 'blips'12.1References13.Proviral DNA load13.1References14.Resistance testing14.1Initial HIV-1 diagnosis14.2ART-naive14.3Post treatment initiation14.4ART-experienced14.5References15.Subtype determination15.1Disease progression15.2Transmission15.3Performance of molecular diagnostic assays15.4Response to therapy15.5Development of drug resistance15.6References16.Other tests to guide use of specific antiretroviral agents16.1Tropism testing16.2HLA B*5701 testing16.3References17.Therapeutic drug monitoring17.1Recommendations17.2References18. Biochemistry testing18.1Introduction18.2Liver function18.3Renal function18.4Dyslipidaemia in HIV-infected individuals18.5Other biomarkers18.6Bone disease in HIV-infected patients18.7References19.Haematology19.1Haemat ological assessment and monitoring19.2Recommendations19.3References20. Serology20.1Overview20.2Hepatitis viruses20.3Herpes viruses20.4Measles and rubella20.5Cytomegalovirus (CMV)20.6References21.Other microbiological screening21.1Tuberculosis screening21.2Toxoplasma serology21.3Tropical screening21.4References22.Sexual health screening including anal and cervical cytology22.1Sexual history taking, counselling and sexually transmitted infection (STI) screening22.2Cervical and anal cytology22.3Recommendations22.4References23.Ro utine monitoring recommended for specific patient groups23.1Women23.2Older age23.3Injecting drug users23.4Individuals coinfected with HBV and HCV23.5Late presenters23.6ReferencesAppendix
ObjectivesLife expectancy is an important indicator informing decision making in policies relating to HIV-infected people. Studies estimating life expectancy after starting combination antiretroviral therapy (cART) have noted differences between income regions. The objective of our study was to perform a meta-analysis to assess life expectancy of HIV-positive people after starting cART, and to quantify differences between low/middle- and high-income countries. MethodsEight cohort studies estimating life expectancy in HIV-positive people initiating cART aged 14 years using the abridged life table method were identified. Random effects meta-analysis was used to pool estimated outcomes, overall and by income region. Heterogeneity between studies was assessed with the I-2 statistic. We estimated additional years of life expected after starting cART at ages 20 and 35 years. ResultsOverall life expectancy in high-income countries was an additional 43.3 years [95% confidence interval (CI) 42.5-44.2 years] and 32.2 years (95% CI 30.9-33.5 years) at ages 20 and 35 years, respectively, and 28.3 (95% CI 23.3-33.3) and 25.6 (95% CI 22.1-29.2) additional years, respectively, in low/middle-income countries. In low/middle-income countries, life expectancy after starting cART at age 20 years was an additional 22.9 years (95% CI 18.4-27.5 years) for men and 33.0 years (95% CI 30.4-35.6 years) for women, but was similar in the two sexes in high-income countries. In all income regions, life expectancy after starting cART increased over calendar time. ConclusionsOur results suggest that the life expectancy of HIV-positive people after starting cART has improved over time. Monitoring life expectancy into the future is important to assess how changes to cART guidelines will affect patient long-term outcomes.
The 2015 Paediatric European Network for Treatment of AIDS (PENTA) guidelines provide practical recommendations on the management of HIV-1 infection in children in Europe and are an update to those published in 2009. Aims of treatment have progressed significantly over the last decade, moving far beyond limitation of short-term morbidity and mortality to optimizing health status for adult life and minimizing the impact of chronic HIV infection on immune system development and health in general. Additionally, there is a greater need for increased awareness and minimization of long-term drug toxicity. The main updates to the previous guidelines include: an increase in the number of indications for antiretroviral therapy (ART) at all ages (higher CD4 thresholds for consideration of ART initiation and additional clinical indications), revised guidance on first- and second-line ART recommendations, including more recently available drug classes, expanded guidance on management of coinfections (including tuberculosis, hepatitis B and hepatitis C) and additional emphasis on the needs of adolescents as they approach transition to adult services. There is a new section on the current ART pipeline' of drug development, a comprehensive summary table of currently recommended ART with dosing recommendations. Differences between PENTA and current US and World Health Organization guidelines are highlighted and explained
BackgroundThe European AIDS Clinical Society (EACS) guidelines are intended for all clinicians involved in the care of HIV-positive persons, and are available in print, online, and as a free App for download for iPhone and Android. Guideline highlightsThe 2015 version of the EACS guidelines contains major revisions in all sections; antiretroviral treatment (ART), comorbidities, coinfections and opportunistic diseases. Among the key revisions is the recommendation of ART for all HIV-positive persons, irrespectively of CD4 count, based on the Strategic Timing of AntiRetroviral Treatment (START) study results. The recommendations for the preferred and the alternative ART options have also been revised, and a new section on the use of pre-exposure prophylaxis (PrEP) has been added. A number of new antiretroviral drugs/drug combinations have been added to the updated tables on drug-drug interactions, adverse drug effects, dose adjustment for renal/liver insufficiency and for ART administration in persons with swallowing difficulties. The revisions of the coinfection section reflect the major advances in anti-hepatitis C virus (HCV) treatment with direct-acting antivirals with earlier start of treatment in individuals at increased risk of liver disease progression, and a phasing out of interferon-containing treatment regimens. The section on opportunistic diseases has been restructured according to individual pathogens/diseases and a new overview table has been added on CD4 count thresholds for different primary prophylaxes. ConclusionsThe diagnosis and management of HIV infection and related coinfections, opportunistic diseases and comorbidities continue to require a multidisciplinary effort for which the 2015 version of the EACS guidelines provides an easily accessable and updated overview
ObjectivesThe Joint United Nations Programme on HIV/AIDS (UNAIDS)/World Health Organization (WHO) 90-90-90 goals propose that 90% of all people living with HIV should know their HIV status, 90% of those diagnosed should receive antiretroviral therapy (ART), and 90% of those should have durable viral suppression. We have estimated the continuum of HIV care for the entire HIV-1-infected population in Sweden. MethodsThe Swedish InfCare HIV Cohort Study collects viral loads, CD4 counts, and viral sequences, along with demographic and clinical data, through an electronic clinical decision support system. Almost 100% of those diagnosed with HIV infection are included in the database, corresponding to 6946 diagnosed subjects living with HIV-1 in Sweden by 31 December 2015. ResultsUsing HIV surveillance data reported to the Public Health Agency of Sweden, it was estimated that 10% of all HIV-infected subjects in Sweden remain undiagnosed. Among all diagnosed patients, 99.8% were linked to care and 97.1% of those remained in care. On 31 December 2015, 6605 of 6946 patients (95.1%) were on ART. A total of 6395 had been on treatment for at least 6 months and 6053 of those (94.7%) had a viral load 73% of all patients living with HIV should be virologically suppressed by 2020. Sweden has already achieved this target, with 78% suppression, and is the first country reported to meet all the UNAIDS/WHO 90-90-90 goals.
Objectives The aims of the study were to describe the clinical presentation and renal and bone abnormalities in a case series of HIV-infected patients receiving treatment with tenofovir (TDF), and to recommend appropriate screening for toxicity related to TDF. Methods Patients were identified from referrals to a specialist HIV renal clinic. Patients were included if treatment with TDF was assessed as the primary cause of the renal function impairment and clinical data were available prior to and following discontinuation of TDF treatment. Data were collected from case note review and clinic databases. Results Twenty-two patients (1.6% of all those who received TDF) were identified with TDF-associated renal toxicity. All had normal serum creatinine prior to TDF therapy. All presented with proteinuria. On stopping TDF, renal function improved. Eight patients had confirmed Fanconi syndrome. Twelve patients presented with bone pain and osteomalacia was confirmed on an isotope bone scan in seven of these patients. The findings (in those patients tested) of tubular proteinuria, reduced tubular transport maximum of phosphate (TmP), and glycosuria were all consistent with the proximal tubule being the site of toxicity. Conclusion Renal toxicity remains a concern in patients treated with TDF. Clinical presentation may be with renal dysfunction, Fanconi syndrome or osteomalacia. Our investigations suggest proximal tubular toxicity as a common pathogenic mechanism.
The aim of the study was to estimate the rates of cardiovascular disease (CVD) events after stopping smoking in patients with HIV infection. Patients who reported smoking status and no previous CVD prior to enrolment in the Data Collection on Adverse Events of Anti-HIV Drugs (D:A:D) study were included in this study. Smoking status is collected at each visit as current smoker (yes/no) and ever smoker (yes/no). Time since stopping smoking was calculated for persons who had reported current smoking during follow-up and no current smoking subsequently. Endpoints were: myocardial infarction (MI); coronary heart disease (CHD: MI plus invasive coronary artery procedure or death from other CHD); CVD (CHD plus carotid artery endarterectomy or stroke); and all-cause mortality. Event rates were calculated for never, previous and current smokers, and smokers who stopped during follow-up. Incidence rate ratios (IRRs) were determined using Poisson regression adjusted for age, sex, cohort, calendar year, family history of CVD, diabetes, lipids, blood pressure and antiretroviral treatment. A total of 27 136 patients had smoking status reported, with totals of 432, 600, 746 and 1902 MI, CHD, CVD and mortality events, respectively. The adjusted IRR of CVD in patients who stopped smoking during follow-up decreased from 2.32 within the first year of stopping to 1.49 after >3 years compared with those who never smoked. Similar trends were observed for the MI and CHD endpoints. Reductions in risk were less pronounced for all-cause mortality. The risk of CVD events in HIV-positive patients decreased with increasing time since stopping smoking. Smoking cessation efforts should be a priority in the management of HIV-positive patients
The overall purpose of these guidelines is to provide guidance on best clinical practice in the treatment and management of human immunodeficiency virus (HIV)-positive pregnant women in the UK. The scope includes guidance on the use of antiretroviral therapy (ART) both to prevent HIV mother-to-child transmission (MTCT) and for the welfare of the mother herself, guidance on mode of delivery and recommendations in specific patient populations where other factors need to be taken into consideration,such as coinfection with other agents. The guidelines are aimed at clinical professionals directly involved with, and responsible for, the care of pregnant women with HIV infection.
Systemic immune activation is a striking consequence of HIV ‐1 infection. Even in virologically suppressed patients, some hyperactivity of the immune system and even of the endothelium and of the coagulation pathway may persist. Apart from immune deficiency, this chronic activation may contribute to various morbidities including atherothrombosis, neurocognitive disorders, liver steatosis and osteoporosis, which are currently main challenges. It is therefore of major importance to better understand the causes and the phenotypes of immune activation in the course of HIV ‐1 infection. In this review we will discuss the various causes of immune activation in HIV ‐1 infected organisms: the presence of the virus together with other microbes, eventually coming from the gut, CD 4+ T cell lymphopenia, senescence and dysregulation of the immune system, and/or genetic factors. We will also describe the activation of the immune system: CD 4+ and CD 8+ T cells, B cells, NKT and NK cells, dendritic cells, monocytes and macrophages, and neutrophils of the inflammation cascade, as well as of the endothelium and the coagulation system. Finally, we will see that antiretroviral therapy reduces the hyperactivity of the immune and coagulation systems and the endothelial dysfunction, but often does not abolish it. A better knowledge of this phenomenon might help us to identify biomarkers predictive of non AIDS ‐linked comorbidities, and to define new strategies aiming at preventing their emergence.
Objectives The aim of the study was to explore the relationships between lymphocyte and monocyte activation, inflammation, and subclinical vascular disease among HIV-1-infected patients on antiretroviral therapy (ART). Methods Baseline mean common carotid artery (CCA) intima-media thickness (IMT) and carotid plaque (IMT>1.5cm) were evaluated in the first 60 subjects enrolled in the Stopping Atherosclerosis and Treating Unhealthy Bone with Rosuvastatin in HIV (SATURN-HIV) trial. All subjects were adults on stable ART with evidence of heightened T-cell activation (CD8+CD38+HLA-DR+19%) or increased inflammation (high-sensitivity C-reactive protein 2mg/L). All had fasting low-density lipoprotein (LDL) cholesterol 130mg/dL. Results Seventy-eight per cent of patients were men and 65% were African-American. Median (interquartile range) age and CD4 count were 47 (43, 52) years and 648 (511, 857) cells/L, respectively. All had HIV-1 RNA<400 HIV-1 RNA copies/mL. Mean CCA-IMT was correlated with log-transformed CD8+CD38+HLA-DR+ percentage (r=0.326; P=0.043), and concentrations of interleukin-6 (r=0.283; P=0.028), soluble vascular cell adhesion molecule (sVCAM; r=0.434; P=0.004), tumour necrosis factor- receptor-I (TNFR-I; r=0.591; P<0.0001) and fibrinogen (r=0.257; P=0.047). After adjustment for traditional cardiovascular disease (CVD) risk factors, the association with TNFR-I (P=0.007) and fibrinogen (P=0.033) remained significant. Subjects with plaque (n=22; 37%) were older [mean (standard deviation) 51 (7.7) vs. 43 (9.4) years, respectively; P=0.002], and had a higher CD8+CD38+HLA-DR+ percentage [median (interquartile range) 31% (24, 41%) vs. 23% (20, 29%), respectively; P=0.046] and a higher sVCAM concentration [mean (standard deviation) 737 (159) vs. 592 (160) ng/mL, respectively; P=0.008] compared with those without plaque. Pro-inflammatory monocyte subsets and serum markers of monocyte activation (soluble CD163 and soluble CD14) were not associated with CCA-IMT or plaque. Conclusions Participants in SATURN-HIV have a high level of inflammation and immune activation that is associated with subclinical vascular disease despite low serum LDL cholesterol.
ObjectivesClinical trials of all-oral direct-acting antivirals (DAAs) for chronic hepatitis C virus (HCV) infection reported high response rates in HCV/HIV coinfection, similar to those obtained in HCV monoinfection. We evaluated the safety and efficacy of these regimens in a clinical practice setting. MethodsIn this prospective observational study, all the HCV-monoinfected and HCV/HIV-coinfected patients undergoing HCV treatment with all-oral DAA regimens in a routine clinical setting from December 2014 to December 2015 were included in the analysis. Sustained virological response 12 weeks after the end of therapy (SVR12) and reported adverse events (AEs) were evaluated. Resistance-associated variants (RAVs) were analysed in a subgroup of patients at baseline and at the time of viral rebound in those with virological failure. ResultsOne-hundred and nine patients (51 HCV-infected and 58 HCV/HIV-coinfected) were enrolled in the study. Sixty per cent had cirrhosis and 52% were pegylated interferon and ribavirin (pegIFN/RBV)-experienced. Thirty-six per cent received ombitasvir + paritaprevir/ritonavir + dasabuvir, 25% sofosbuvir + daclatasvir, 16% sofosbuvir + simeprevir, 17% sofosbuvir + ribavirin and 6% sofosbuvir + ledipasvir; ribavirin was used in 57% of subjects. The SVR12 rate was 91% and 96% in HIV-infected and uninfected patients, respectively (P = 0.44). The 4-week HCV viral decline was similar in the two groups. RAVs were found at baseline in 23 of 49 patients and did not affect SVR12. No predictors of SVR12 were identified in our cohort. ConclusionsTreatment with all-oral DAA combinations of patients infected with HCV and with HCV/HIV under real-life conditions led to high and similar rates of SVR12. Moreover, the historical factors associated with a sustained virological response to pegIFN/RBV were not predictive of the response to all-oral DAAs.