AIDS (London, England) (AIDS )

Publisher: Lippincott, Williams & Wilkins

Journal description

Current impact factor: 6.56

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013/2014 Impact Factor 6.557
2012 Impact Factor 6.407
2011 Impact Factor 6.245
2010 Impact Factor 6.348
2009 Impact Factor 4.909
2008 Impact Factor 5.46

Impact factor over time

Impact factor

Additional details

5-year impact 0.00
Cited half-life 6.00
Immediacy index 1.15
Eigenfactor 0.07
Article influence 1.83
Other titles AIDS (London, England: Online)
ISSN 1473-5571
OCLC 225537630
Material type Periodical, Internet resource
Document type Internet Resource, Journal / Magazine / Newspaper

Publisher details

Lippincott, Williams & Wilkins

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    • NIH authors will have their accepted manuscripts transmitted to PubMed Central on their behalf after a 12 months embargo (see policy for details)
    • Wellcome Trust and HHMI authors will have their accepted manuscripts transmitted to PubMed Central on their behalf after a 6 months embargo (see policy for details)
    • If the hybrid open access option is not available, RCUK authors articles will be released as Creative Commons Attirbution Non-Commercial No Derivatives after a 6 months
    • Publisher last reviewed on 10/04/2014
  • Classification
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Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: To estimate the prevalence of the HIV-1 subtype B pandemic (BPANDEMIC) and Caribbean (BCAR) clades in Latin America and to reconstruct the spatiotemporal dynamics of dissemination of the BCAR clades in the region. A total of 7654 HIV-1 subtype B pol sequences collected from 18 different Latin American countries between 1989 and 2011 were analyzed together with subtype B reference sequences representative of the BPANDEMIC (US/France = 300) and the BCAR (Caribbean = 279, Panama = 37) clades. Phylogeographic and evolutionary parameters were estimated from sequence data using maximum likelihood and Bayesian coalescent-based methods. Nonpandemic BCAR strains were probably disseminated from the Caribbean islands of Hispaniola and Trinidad and Tobago into Latin America since the early 1970s. The BCAR strains reached nearly all countries from Latin America here analyzed and in some of them were spread locally, although their overall prevalence in the region is low. The BPANDEMIC clade comprises more than 90% of subtype B infections in most countries analyzed, with exception of Suriname, French Guyana and probably Guyana, where both BPANDEMIC and BCAR clades seem to circulate at a similar prevalence. This study demonstrates that nonpandemic subtype B lineages of Caribbean origin have been disseminated into Latin America shortly after the estimated introduction of subtype B in the continent. Despite their early dissemination, the BCAR strains account for a minor fraction of current HIV-1 subtype B infections in the region that are mainly driven by spreading of the globally disseminated BPANDEMIC clade.
    AIDS (London, England) 02/2015; 29(4):483-92.
  • AIDS (London, England) 02/2015; 29(4):504-6.
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    ABSTRACT: To investigate the impact of HAART-induced HIV suppression on levels of 24 serological biomarkers of inflammation and immune activation. A prospective cohort study. Biomarkers were measured with multiplex assays in centralized laboratories using stored serum samples contributed by 1697 men during 8903 person-visits in the Multicenter AIDS Cohort Study (MACS) from 1984 to 2009. Using generalized gamma models, we compared biomarker values across three groups, adjusting for possible confounders: HIV-uninfected (NEG); HIV-positive, HAART-naive (NAI); and HAART-exposed with HIV RNA suppressed to less than 50 copies/ml plasma (SUP). We also estimated changes in biomarker levels associated with duration of HIV suppression, using splined generalized gamma regression with a knot at 1 year. Most biomarkers were relatively normalized in the SUP group relative to the NAI group; however, 12 biomarkers in the SUP group were distinct (P < 0.002) from NEG values: CXCL10, C-reactive protein (CRP), sCD14, sTNFR2, tumour necrosis factor-alpha (TNF-α), sCD27, sGP130, interleukin (IL)-8, CCL13, BAFF, GM-CSF and IL-12p70. Thirteen biomarkers exhibited significant changes in the first year after viral suppression, but none changed significantly after that time. Biomarkers of inflammation and immune activation moved towards HIV-negative levels within the first year after HAART-induced HIV suppression. Although several markers of T-cell activation returned to levels present in HIV-negative men, residual immune activation, particularly monocyte/macrophage activation, was present. This residual immune activation may represent a therapeutic target to improve the prognosis of HIV-infected individuals receiving HAART.
    AIDS (London, England) 02/2015; 29(4):463-71.
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    ABSTRACT: Neutralizing antibodies against HIV-1 such as a humanized mAb KD-247 can mediate effector functions that attack infected cells in vitro. However, the clinical efficacy of neutralizing antibodies in infected individuals remains to be determined. We evaluated the safety, tolerability and pharmacokinetics of KD-247 infusion and its effect on plasma HIV-1 RNA load and CD4 T-cell count. KD-1002 is a phase Ib, double-blind, placebo-controlled, dose-escalation study of KD-247 in asymptomatic HIV-1 seropositive individuals who did not need antiretroviral therapy. Individuals were randomized to 4, 8 or 16 mg/kg KD-247 or placebo, and received three infusions over a 2-week period. Patients were randomized to receive one of the three doses of KD-247 and the treatment was well tolerated. We observed a significant decrease in HIV RNA in the 8 and 16 mg/kg KD-247 cohorts, with two individuals who achieved more than 1 log reduction of HIV RNA. Two patients in the 16 mg/kg cohort had selections and/or mutations in the V3-tip region that suggested evasion of neutralization. Long-term suppression of viral load was observed in one patient despite a significant decrease in plasma concentration of KD-247, suggesting effects of the antibody other than neutralization or loss of fitness of the evading virus. The results indicate that KD-247 reduces viral load in patients with chronic HIV-1 infection and further clinical trials are warranted.
    AIDS (London, England) 02/2015; 29(4):453-62.
  • AIDS (London, England) 02/2015; 29(4):395-400.
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    ABSTRACT: All-cause mortality and serious non-AIDS events (SNAEs) in individuals with HIV-1 infection receiving antiretroviral therapy are associated with increased production of interleukin-6 which appears to be driven by monocyte/macrophage activation. Plasma levels of other cytokines or chemokines associated with immune activation might also be biomarkers of an increased risk of mortality and/or SNAEs. Baseline plasma samples from 142 participants enrolled into the Strategies for Management of Antiretroviral Therapy study, who subsequently died, and 284 matched controls, were assayed for levels of 15 cytokines and chemokines. Cytokine and chemokine levels were analysed individually and when grouped according to function (innate/proinflammatory response, cell trafficking and cell activation/proliferation) for their association with the risk of subsequent death. Higher plasma levels of proinflammatory cytokines (interleukin-6 and tumour necrosis factor-α) were associated with an increased risk of all-cause mortality but in analyses adjusted for potential confounders, only the association with interleukin-6 persisted. Increased plasma levels of the chemokine CXCL8 were also associated with all-cause mortality independently of hepatitis C virus status but not when analyses were adjusted for all confounders. In contrast, higher plasma levels of cytokines mediating cell activation/proliferation were not associated with a higher mortality risk and exhibited a weak protective effect when analysed as a group. Whereas plasma levels of interleukin-6 are the most informative biomarker of cytokine dysregulation associated with all-cause mortality in individuals with HIV-1 infection, assessment of plasma levels of CXCL8 might provide information about causes of mortality and possibly SNAEs.
    AIDS (London, England) 02/2015;
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    ABSTRACT: HIV is a major public health problem among MSM in the United Kingdom with around 2400 new infections annually. We quantified the contribution of biological and behavioural factors. Modelling study. A partnership-based model of HIV transmission among UK MSM aged 15-64 years was developed and calibrated to time series HIV prevalence. The calibration was validated using multiple surveillance datasets. Population-attributable fractions were used to estimate the contribution of behavioural and biological factors to HIV transmission over the period 2001-2002, 2014-2015, and 2019-2020. The contribution of most biological and behavioural factors was relatively constant over time, with the key group sustaining HIV transmission being higher-sexual activity MSM aged below 35 years living with undiagnosed HIV. The effect of primary HIV infection was relatively small with 2014-2015 population-attributable fraction of 10% (3-28%) in comparison with other subsequent asymptomatic stages. Diagnosed men who were not on antiretroviral therapy (ART) currently contributed 26% (14-39%) of net infections, whereas ART-treated MSM accounted for 17% (10-24%). A considerable number of new infections are also likely to occur within long-term relationships. The majority of the new HIV infections among MSM in the United Kingdom during 2001-2020 is expected to be accounted for by a small group of younger and highly sexually active individuals, living with undiagnosed HIV in the asymptomatic stage. Bringing this group into HIV/AIDS care by improving testing uptake is a vital step for preventing onward transmission and will determine the success of using ART as prevention.
    AIDS (London, England) 01/2015; 29(3):339-49.
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    ABSTRACT: Increased risk of cardiovascular disease in patients infected with HIV has been attributed to immune activation, inflammation, and immunosenescence, all of which are linked to chronic immune activation by viral infections, particularly cytomegalovirus (CMV). Our aim is to evaluate the impact of these atherogenic markers in HIV-infected patients who never smoked. Exposure-matched, cross-sectional study. In 59 HIV-infected individuals [n = 30 undergoing ≥4 years of antiretroviral therapy (ART); n = 29 never treated with ART] and 30 age-matched HIV-negative controls, we measured the level of activation and senescence, as well as the frequency of CMV-specific T cells, on peripheral blood mononuclear cells, while examining their association with carotid intima-media thickness. Partial correlations were adjusted for age, systolic blood pressure, and nadir CD4 cell count. The previously described roles of T-cell activation, CMV, and immunosenescence in the atherosclerotic risk of HIV-infected patients, as assessed by carotid intima-media thickness, were not apparent in our cohort of particularly 'healthy' HIV-infected never-smokers. In HIV-infected individuals at low cardiovascular disease risk, our data show that the increased risk of carotid atherosclerosis is not associated with immunological markers described to be associated with HIV disease progression.
    AIDS (London, England) 01/2015; 29(3):287-93.
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    ABSTRACT: To determine the effect of virally suppressive antiretroviral therapy (ART) on cortical neurodegeneration and associated neurocognitive impairment. Retrospective, postmortem observational study. Clinical neuropsychological and postmortem neuropathology data were analyzed in 90 HIV-infected volunteers from the general community who had never undergone ART (n = 7, 'naive') or who had undergone ART and whose plasma viral load was detectable (n = 64 'unsuppressed') or undetectable (n = 19, 'suppressed') at the last clinical visit before death. Individuals were predominately men (74/90, 82%) with a mean age of 44.7 years (SD 9.8). Cortical neurodegeneration was quantified by measuring microtubule-associated protein (MAP2) and synaptophysin (SYP) density in midfrontal cortex tissue sections. The suppressed group had higher SYP density than the naive group (P = 0.007) and higher MAP2 density than the unsuppressed group (P = 0.04). The suppressed group had lower odds of HIV-associated neurocognitive disorders than naive [odds ratio (OR) 0.07, P = 0.03]. Higher SYP was associated with lower likelihood of HIV-associated neurocognitive disorders in univariable (OR 0.8, P = 0.03) and multivariable models after controlling for ART and brain HIV p24 protein levels (OR 0.72, P = 0.01). We conclude that virally suppressive ART protects against cortical neurodegeneration. Further, we find evidence supporting the causal chain from treatment-mediated peripheral and central nervous system viral load suppression to reduced neurodegeneration and improved neurocognitive outcomes.
    AIDS (London, England) 01/2015; 29(3):323-30.
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    ABSTRACT: HIV-infected participants are at a higher risk for cardiovascular disease (CVD). N-terminal pro-B-type natriuretic peptide (NT-proBNP) is a significant predictor of CVD in the general population and is associated with mortality in HIV. The 96-week Stopping Atherosclerosis and Treating Unhealthy Bone with Rosuvastatin in HIV (SATURN-HIV) trial randomized 147 patients on stable antiretroviral therapy with low-density lipoprotein-cholesterol level lower than 130 mg/dl and without overt heart failure to 10 mg daily rosuvastatin or placebo. We measured NT-proBNP levels by enzyme-linked immunosorbent assay (ELISA). Baseline and changes in NT-proBNP were compared between groups. Spearman correlation was used to explore relationships between baseline NT-proBNP, inflammation, and CVD risk markers. Multivariable analyses were conducted to assess associations with NT-proBNP levels. Median age was 46 years, 80% were men, 69% were African American, and 46% were on protease inhibitors. At baseline, median (Q1, Q3) NT-proBNP was higher in the rosuvastatin group than placebo [41 (20, 66.5) versus 25 pg/ml (11, 56), P = 0.012)]. Baseline NT-proBNP correlated with bulb and common carotid artery intima-media thickness, coronary calcium score, interleukin 6, and cystatin C. After 96 weeks, median NT-proBNP decreased significantly in the rosuvastatin group versus placebo (-1.50 versus +4.50 pg/ml, P = 0.041). Within the rosuvastatin group, changes in NT-proBNP were negatively correlated with changes in insulin resistance and total limb fat. Rosuvastatin reduces plasma NT-proBNP in HIV-infected participants on antiretroviral therapy. NT-proBNP correlated with several measures of CVD risk, independent of inflammation markers.
    AIDS (London, England) 01/2015; 29(3):313-21.
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    ABSTRACT: Thirty-six months of isoniazid preventive therapy (36IPT) was superior to 6 months of IPT (6IPT) in preventing tuberculosis (TB) among HIV-infected adults in Botswana. We assessed the posttrial durability of this benefit. A 36-month double-blind placebo controlled trial (1 : 1 randomization) with recruitment between November 2004 and July 2006 and observation until June 2011. One thousand, nine hundred and ninety-five participants were followed in eight public health clinics. Twenty-four percent had a tuberculin skin test ≥5 mm (TST-positive). A minimum CD4 lymphocyte count was not required for enrolment. Antiretroviral therapy (ART) was provided in accordance with Botswana guidelines; 72% of participants retained by June 2011 had initiated ART. Multivariable analysis using Cox regression analysis included treatment arm, TST status, ART as a time-dependent variable and CD4 cell count at baseline and updated at 36 months. In the posttrial period, 2.13 and 2.14 per 100 person-years accumulated, whereas 0.93 and 1.13% TB incidence rates were observed in the 36IPT and 6IPT arms, respectively (P = 0.52). The crude hazard ratio of TB during the trial and posttrial was 0.57 [95% confidence intervals (CI) 0.33, 0.99] and 0.82 (95% CI 0.46, 1.49), and when restricted to TST-positive participants was 0.26 (95% CI 0.08, 0.80) and 0.40 (95% CI 0.15, 1.08), respectively. Multivariable analysis showed that ART use was associated with reduced death (adjusted hazard ratio 0.36, 95% CI 0.17-0.75) but not TB (0.92, 95% CI 0.55-1.53) in the posttrial period. The benefit of 36IPT for TB prevention declined posttrial in this cohort. Adjunctive measures are warranted to prevent TB among HIV-infected persons receiving long-term ART in TB-endemic settings.
    AIDS (London, England) 01/2015; 29(3):351-9.
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    ABSTRACT: Many HIV patients on antiretroviral therapy have controlled viremia and restored (albeit partially) immunity. Yet, they have high rates of lung cancer, even after controlling for smoking. We tested the hypothesis that HIV proteins accelerate development/progression of lung cancer in an immunocompetent HIV transgenic mouse model. The expression of HIV proteins did not enhance lung tumorigenesis caused by two different tobacco carcinogens, suggesting that incompletely restored immunity and/or inflammation, which persist(s) in most HIV patients despite controlled viremia, underlie(s) excess risk of lung cancer. Adjuvant therapies that restore immunity and lower inflammation may decrease lung cancer mortality in HIV patients.
    AIDS (London, England) 01/2015;
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    ABSTRACT: Faldaprevir is a potent, once-daily hepatitis C virus (HCV) NS3/4A protease inhibitor. STARTVerso4 assessed the efficacy and safety of faldaprevir and response-guided pegylated interferon α-2a/ribavirin (PegIFN/RBV) in individuals with HCV/HIV co-infection. A phase 3 open-label study (NCT01399619). Individuals (N = 308) co-infected with HCV genotype 1 (treatment-naïve or prior interferon relapsers) and HIV [96% on antiretroviral therapy (ART)] received faldaprevir 120 mg (N = 123) or 240 mg (N = 185) and PegIFN/RBV. Those receiving a protease inhibitor or efavirenz ART were assigned to faldaprevir 120 or 240 mg, respectively. Individuals achieving early treatment success (ETS; HCV RNA <25 IU/ml at week 4 and undetectable at week 8) were randomized to 24 or 48 weeks of PegIFN/RBV. The primary endpoint was sustained virologic response 12 weeks after treatment (SVR12). SVR12 was achieved in 221 (72%) individuals, and the rates were comparable across faldaprevir doses. ETS was achieved in 80%, and of these 86% achieved SVR12, with comparable rates with 24 and 48 weeks of PegIFN/RBV (87 and 94%, respectively). In multivariate analysis, age below 40 years, IL28B CC genotype, and baseline HCV RNA below 800 000 IU/ml were associated with SVR12 (P = 0.027, P < 0.0001, and P = 0.0002, respectively), whereas treatment (ART regimen and faldaprevir dose), liver cirrhosis, and genotype 1 subtype were not. The safety profile was comparable to that of faldaprevir in HCV-monoinfected individuals. High SVR12 rates were achieved with faldaprevir and PegIFN/RBV in HIV/HCV co-infected individuals, regardless of faldaprevir dose and background ART, HCV genotype 1 subtype, or cirrhosis status. SVR rates mirrored those obtained with similar regimens in HCV monoinfected individuals.
    AIDS (London, England) 01/2015;
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    ABSTRACT: Despite the use of HAART to control HIV, systemic immune activation and inflammation persists with the consequence of developing serious non-AIDS events. The mechanisms that contribute to persistent systemic immune activation have not been well defined. The intestine is the major source of "sterile" inflammation and plays a critical role in immune function; thus, we sought to determine whether intestinal gene expression was altered in virally controlled HIV+ individuals. Gene expression was compared in biopsy samples collected from HIV- and HIV+ individuals from the ileum, right colon (ascending colon), and left colon (sigmoid). Affymetrix gene arrays were performed on tissues and pathway analyses were conducted. Gene expression was correlated with systemic markers of intestinal barrier dysfunction and inflammation and intestinal microbiota composition. Genes involved in cellular immune response, cytokine signaling, pathogen-influenced signaling, humoral immune response, apoptosis, intracellular and second messenger signaling, cancer, organismal growth and development, and proliferation and development were upregulated in the intestine of HIV+ individuals with differences observed in the ileum, right, and left colon. Gene expression in the ileum primarily correlated with systemic markers of inflammation (e.g., IL7R, IL2, and TLR2 with serum TNF) whereas expression in the colon correlated with the microbiota community (e.g., IFNG, IL1B, and CD3G with Bacteroides). These data demonstrate persistent, proinflammatory changes in the intestinal mucosa of virally suppressed HIV+ individuals. These changes in intestinal gene expression may be the consequence of or contribute to barrier dysfunction and intestinal dysbiosis observed in HIV.
    AIDS (London, England) 01/2015;
  • AIDS (London, England) 01/2015; 29(2):246-8.