AIDS (London, England) (AIDS )

Publisher: Lippincott, Williams & Wilkins

Description

Impact factor 6.56

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    Impact factor
  • 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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    • 12 months embargo
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    • Published source must be acknowledged with full citation
    • Set statement to accompany deposit
    • Must link to publisher version
    • 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
    ​ yellow

Publications in this journal

  • Shigeru Kawabata, Alonso Heredia, Joell Gills, Robert R Redfield, Phillip A Dennis, Joseph Bryant
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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;
  • Douglas Dieterich, Mark Nelson, Vicente Soriano, Keikawus Arastéh, Josep M Guardiola, Jürgen K Rockstroh, Sanjay Bhagani, Montserrat Laguno, Cristina Tural, Patrick Ingiliz, Mamta K Jain, Jerry O Stern, Montserrat Manero, Richard Vinisko, Jens Kort
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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;
  • Mohamed Abdel-Mohsen, Charlene Wang, Matthew C Strain, Steven M Lada, Xutao Deng, Leslie R Cockerham, Christopher D Pilcher, Frederick M Hecht, Teri Liegler, Douglas D Richman, Steven G Deeks, Satish K Pillai
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    ABSTRACT: The eradication of HIV necessitates elimination of the HIV latent reservoir. Identifying host determinants governing latency and reservoir size in the setting of antiretroviral therapy (ART) is an important step in developing strategies to cure HIV infection. We sought to determine the impact of cell-intrinsic immunity on the HIV latent reservoir. We investigated the relevance of a comprehensive panel of established anti-HIV-1 host restriction factors to multiple established virologic and immunologic measures of viral persistence in HIV-1-infected, ART-suppressed individuals. We measured the mRNA expression of 42 anti-HIV-1 host restriction factors, levels of cell-associated HIV-1 RNA, levels of total pol and 2-long terminal repeat (2-LTR) circle HIV-1 DNA and immunophenotypes of CD4 T cells in 72 HIV-1-infected individuals on suppressive ART (23 individuals initiated ART less than 1 year postinfection, and 49 individuals initiated ART greater than 1 year post-infection). Correlations were analysed using nonparametric tests. The enhanced expression of a few select host restriction factors, p21, schlafen 11 and PAF1, was strongly associated with reduced CD4 T-cell associated HIV RNA during ART (P < 0.001). In addition, our data suggested that ART perturbs the regulatory relationship between CD4 T-cell activation and restriction factor expression. Lastly, cell-intrinsic immune responses were significantly enhanced in individuals who initiated ART during early versus chronic infection and may contribute to the reduced reservoir size observed in these individuals. Intrinsic immune responses modulate HIV persistence during suppressive ART and may be manipulated to enhance the efficacy of ART and promote viral eradication through reversal of latency in vivo.
    AIDS (London, England) 01/2015;
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    ABSTRACT: Postnatal HIV-1 mother-to-child transmission (MTCT) occurs in spite of antiretroviral therapy. Co-infections in breast milk with cytomegalovirus (CMV) and Epstein-Barr virus (EBV) are associated with increased HIV-1 shedding in this compartment. We investigated CMV levels and EBV detection in breast milk as potential risk factors for MTCT of HIV-1 via breastfeeding. Cell-free HIV-1 RNA, cell-associated HIV-1 DNA, CMV and EBV DNA were quantified in breast milk from 62 HIV-infected mothers and proven postnatal MTCT of HIV-1 via breastfeeding. Controls were 62 HIV-positive mothers with HIV-uninfected infants. Median (interquartile range) CMV DNA viral load was significantly higher in cases [88 044 (18 586-233 904)] than in controls [11 167 (3221-31 152)] copies/10 breast milk cells (P < 0.001). Breast milk CMV DNA level correlated positively with breast milk HIV-1 RNA level in cases and controls. EBV DNA was detectable in a higher proportion of breast milk samples of cases (37.1%) than controls (16.1%; P = 0.009). HIV-1 MTCT was strongly associated with HIV-1 RNA shedding in breast milk and plasma. In multivariable analysis, every 1 log10 increase in breast milk CMV DNA was associated with a significant 2.5-fold greater odds of MTCT of HIV-1, independent of breast milk and plasma HIV-1 levels; the nearly three-fold increased risk of HIV-1 MTCT with breast milk EBV DNA detection did not reach significance. We provide the first evidence of an independent association between CMV in breast milk, and postnatal MTCT of HIV-1. This association could fuel persistent shedding of HIV-1 in breast milk in women receiving antiretroviral therapy. EBV DNA detection in breast milk may also be associated with MTCT of HIV-1, but only marginally so.
    AIDS (London, England) 01/2015; 29(2):145-53.
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    ABSTRACT: The objective of this study is to assess the effect of maternal HIV and Mycobacterium tuberculosis (Mtb) infection on cellular responses to bacille Calmette-Guérin (BCG) immunization. A mother-infant cohort study. Samples were collected from mother-infant pairs at delivery. Infants were BCG-vaccinated at 6 weeks of age and a repeat blood sample was collected from infants at 16 weeks of age. BCG-specific T-cell proliferation and intracellular cytokine expression were measured by flow cytometry. Secreted cytokines and chemokines in cell culture supernatants were analysed using a Multiplex assay. One hundred and nine (47 HIV-exposed and 62 HIV-unexposed) mother-infants pairs were recruited after delivery and followed longitudinally. At birth, proportions of mycobacteria-specific proliferating T cells were not associated with either in-utero HIV exposure or maternal Mtb sensitization. However, in-utero HIV exposure affected infant-specific T-cell subsets [tumour necrosis factor-alpha (TNF-α) single positive proliferating CD4 T cells and interferon-gamma (IFN-γ), TNF-α dual-positive CD4 T cells]. Levels of TNF-α protein in cell culture supernatants were also significantly higher in HIV-exposed infants born to Mtb-sensitized mothers. In the presence of maternal Mtb sensitization, frequencies of maternal and newborn BCG-specific proliferating CD4 T cells were positively correlated. Following BCG vaccination, there was no demonstrable effect of HIV exposure or maternal Mtb infection on infant BCG-specific T-cell proliferative responses or concentrations of secreted cytokines and chemokines. Effects of maternal HIV and Mtb infection on infant immune profiles at birth are transient only, and HIV-exposed, noninfected infants have the same potential to respond to and be protected by BCG vaccination as HIV-unexposed infants.
    AIDS (London, England) 01/2015; 29(2):155-65.
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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.
  • AIDS (London, England) 01/2015; 29(2):248-50.
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    ABSTRACT: The objective of this study is to assess whether multivariate normative comparison (MNC) improves detection of HIV-1 associated neurocognitive disorder (HAND) as compared with Frascati and Gisslén criteria. :One-hundred and three HIV-1 infected men with suppressed viremia on combination antiretroviral therapy (cART) for at least 12 months and 74 HIV-uninfected male controls (comparable regarding age, ethnicity, sexual orientation, premorbid intelligence and educational level), aged at least 45 years, underwent neuropsychological assessment covering six cognitive domains (fluency, attention, information processing speed, executive function, memory and motor function). Frascati and Gisslén criteria were applied to detect HAND. Next, MNC was performed to compare the cognitive scores of each HIV-positive individual against the cognitive scores of the control group. HIV-infected men showed significantly worse performance on the cognitive domains of attention, information processing speed and executive function compared with HIV-uninfected controls. HAND by Frascati criteria was highly prevalent in HIV-infected [48%; 95% confidence interval (95% CI) 38-58] but nearly equally so in HIV-uninfected men (36%; 95% CI 26-48), confirming the low specificity of this method. Applying Gisslén criteria, HAND-prevalence was reduced to 5% (95% CI 1-9) in HIV-infected men and to 1% (95% CI 1-3) among HIV-uninfected controls, indicating better specificity but reduced sensitivity. MNC identified cognitive impairment in 17% (95% CI 10-24) of HIV-infected men and in 5% (95% CI 0-10) of the control group (P = 0.02, one-tailed), showing an optimal balance between sensitivity and specificity. Prevalence of cognitive impairment in HIV-1 infected men with suppressed viremia on cART estimated by MNC was much higher than that estimated by Gisslén criteria, although the false positive rate was greatly reduced compared with the Frascati criteria. VIDEO ABSTRACT::
    AIDS (London, England) 01/2015;
  • AIDS (London, England) 01/2015; 29(2):239-40.
  • AIDS (London, England) 01/2015; 29(2):245-6.
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    ABSTRACT: The objective of this study is to understand how trends in HIV acquisition among youth can be influenced by change in HIV risk factors, social factors and prevention and treatment programmes. Trends in HIV incidence (per 1000 person-years), by sex and age group, were estimated using data from youth (15-24 years: n = 22 164) in the Rakai Community Cohort Study. Trends in HIV incidence were compared with trends in previously identified HIV risk factors, social factors and programmes. Poisson and linear regression were used to test for statistical significance and decomposition was used to calculate attribution of risk factors to HIV incidence. Substantial declines between 1999 and 2011 occurred in sexual experience, multiple partners and sexual concurrency among adolescents and young adults. HIV acquisition declined substantially (86%, P = 0.006) among adolescent women (15-19 years) but not among men or young adult women. Changes in HIV incidence and risk behaviours coincided with increases in school enrolment, decline in adolescent marriage, availability of antiretroviral therapy (ART) and increases in male medical circumcision (MMC). Much of the decline in HIV incidence among adolescent women (71%) was attributable to reduced sexual experience; the decline in sexual experience was primarily attributable to increasing levels of school enrolment. Dramatic decreases in HIV incidence occurred among adolescent women in Rakai. Changes in school enrolment and sexual experience were primarily responsible for declining HIV acquisition over time among adolescent women. Given limited improvement among young men and young adult women, the need for effective HIV prevention for young people remains critical.
    AIDS (London, England) 01/2015; 29(2):211-9.
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    ABSTRACT: To test a novel social network HIV risk-reduction intervention for MSM in Russia and Hungary, where same-sex behavior is stigmatized and men may best be reached through their social network connections. A 2-arm trial with 18 sociocentric networks of MSM randomized to the social network intervention or standard HIV/STD testing/counseling. St. Petersburg, Russia and Budapest, Hungary. Eighteen 'seeds' from community venues invited the participation of their MSM friends who, in turn, invited their own MSM friends into the study, a process that continued outward until eighteen three-ring sociocentric networks (mean size = 35 members, n = 626) were recruited. Empirically identified network leaders were trained and guided to convey HIV prevention advice to other network members. Changes in sexual behavior from baseline to 3-month and 12-month follow-up, with composite HIV/STD incidence, measured at 12 months to corroborate behavior changes. There were significant reductions between baseline, first follow-up, and second follow-up in the intervention versus comparison arm for proportion of men engaging in any unprotected anal intercourse (UAI) (P = 0.04); UAI with a nonmain partner (P = 0.04); and UAI with multiple partners (P = 0.002). The mean percentage of unprotected anal intercourse acts significantly declined (P = 0.001), as well as the mean number of UAI acts among men who initially had multiple partners (P = 0.05). Biological HIV/STD incidence was 15% in comparison with condition networks and 9% in intervention condition networks. Even where same-sex behavior is stigmatized, it is possible to reach MSM and deliver HIV prevention through their social networks.
    AIDS (London, England) 01/2015;
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    ABSTRACT: There are several published systematic reviews of adult retention in care after antiretroviral therapy (ART) initiation among adults, but limited information on pediatric retention. Systematic review of pediatric retention on ART in low and middle-income countries during 2008-2013. We estimated all-cause attrition (death and loss to follow-up) and retention for pediatric patients receiving first-line ART in routine settings. We searched PubMed, Embase, Cochrane Register, and ISI Web of Science (January 2008-December 2013) and abstracts from AIDS and IAS (2008-2013). We estimated mean retention across cohorts using simple averages; interpolated any time period not reported to, up to the last period reported; summarized total retention in the population using Kaplan-Meier survival curves; and compared pediatric to adult retention. We found 39 reports of retention in 45 patient cohorts and 55 904 patients in 23 countries. Among them, 37% of patients not retained in care were known to have died and 63% were lost to follow-up. Unweighted averages of reported retention were 85, 81, and 81% at 12, 24, and 36 months after ART initiation. From life-table analysis, we estimated retention at 12, 24, and 36 months at 88, 72, and 67%. We estimated 36-month retention at 66% in Africa and 74% in Asia. Pediatric ART retention was similar to that among adults. There were limited data from Asia, only one study from Latin America and the Caribbean, and no data from Eastern Europe, Central Asia, or the Middle East.
    AIDS (London, England) 01/2015;
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    ABSTRACT: The longitudinal trajectories that individuals may take from a state of normal cognition to HIV-associated dementia are unknown. We applied a novel statistical methodology to identify trajectories to cognitive impairment, and factors that affected the 'closeness' of an individual to one of the canonical trajectories. The Multicenter AIDS Cohort Study (MACS) is a four-site longitudinal study of the natural and treated history of HIV disease among gay and bisexual men. Using data from 3892 men (both HIV-infected and HIV-uninfected) enrolled in the neuropsychology substudy of the MACS, a Mixed Membership Trajectory Model (MMTM) was applied to capture the pathways from normal cognitive function to mild impairment to severe impairment. MMTMs allow the data to identify canonical pathways and to model the effects of risk factors on an individual's 'closeness' to these trajectories. First, we identified three distinct trajectories to cognitive impairment: 'normal aging' (low probability of mild impairment until age 60); 'premature aging' (mild impairment starting at age 45-50); and 'unhealthy' (mild impairment in 20s and 30s) profile. Second, clinically defined AIDS, and not simply HIV disease, was associated with closeness to the premature aging trajectory. And, third, hepatitis-C infection, depression, race, recruitment cohort and confounding conditions all affected individual's closeness to these trajectories. These results provide new insight into the natural history of cognitive dysfunction in HIV disease and provide evidence for a potential difference in the pathophysiology of the development of cognitive impairment based on trajectories to impairment.
    AIDS (London, England) 01/2015;
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    ABSTRACT: Some intestinal microbiota-generated metabolites of phosphatidylcholine are recognized to be proatherogenic. As the HIV population is vulnerable to cardiovascular disease and can develop intestinal dysbiosis associated with systemic inflammation, we investigated the novel relationship between microbiota-derived metabolites of phosphatidylcholine and coronary atherosclerosis in HIV. One hundred and fifty-five HIV-infected and 67 non-HIV-infected individuals without known history of cardiovascular disease were previously recruited to assess coronary plaque by computed tomography angiography. In the current study, we evaluate whether serum choline, trimethylamine (TMA), or trimethylamine-N-oxide (TMAO) levels are associated with plaque features. Young, asymptomatic HIV-infected patients (age 47 ± 7 years) demonstrated significantly higher prevalence of plaque (53 vs. 35%, P = 0.01) and number of total plaque segments (1.8 ± 2.5 vs. 1.2 ± 2.2, P = 0.03) when compared with well matched noninfected individuals with similar comorbidities. TMA was significantly associated with calcium score (r = 0.22, P = 0.006), number of total (r = 0.20, P = 0.02) and calcified (r = 0.18, P = 0.03) plaque segments, and calcium plaque volume (r = 0.19, P = 0.02) and mass (r = 0.22, P = 0.009) in the HIV cohort only. In multivariate modeling among HIV-infected patients, TMA remained significantly associated with calcium score (P = 0.008), number of total (P = 0.005) and calcified (P = 0.02) plaque segments, and calcium plaque volume (P = 0.01) and mass (P = 0.007), independent of Framingham risk score. In contrast, there was no association of TMAO to coronary plaque features in either cohort. A link between TMA and atherosclerosis has not previously been established. The current study suggests that TMA may be a nontraditional risk factor related to the number of plaque segments and severity of calcified plaque burden in HIV.
    AIDS (London, England) 01/2015;
  • AIDS (London, England) 01/2015; 29(1):125-7.
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    ABSTRACT: T20 (Enfuvirtide), which is a 36-residue peptide derived from the C-terminal heptad repeat (CHR) of gp41, is the only clinically available HIV-1 fusion inhibitor, but it easily induces drug resistance, which calls for next-generation drugs. We recently demonstrated that the M-T hook structure can be used to design a short CHR peptide that specifically targets the conserved gp41 pocket rather than the T20-resistant sites. We attempted to develop more potent HIV-1 fusion inhibitors based on the structure-activity relationship of MT-SC22EK. Multiple biophysical and functional approaches were performed to determine the structural features, binding affinities and anti-HIV activities of the inhibitors. The 23-residue peptide HP23, which mainly contains the M-T hook structure and pocket-binding sequence, showed a helical and trimeric state in solution. HP23 had dramatically improved binding stability and antiviral activity, and it was the most potent inhibitor of the M-T hook-modified and unmodified control peptides. More promisingly, HP23 was highly active in the inhibition of diverse HIV-1 subtypes, including T20 and MT-SC22EK resistant HIV-1 mutants, and it exhibited a high genetic barrier to the development of resistance. Our studies delivered an ideal HIV-1 fusion inhibitor that specifically targeted the highly conserved gp41 pocket and possessed potent binding and antiviral activity. Furthermore, HP23 can serve as a critical tool to explore the mechanisms of HIV-1 fusion and inhibition.
    AIDS (London, England) 01/2015; 29(1):13-21.
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    ABSTRACT: Viral load and CD4% are often not available in resource-limited settings for monitoring children's responses to antiretroviral therapy (ART). We aimed to construct normative curves for weight gain at 6, 12, 18, and 24 months following initiation of ART in children, and to assess the association between poor weight gain and subsequent responses to ART. Analysis of data from HIV-infected children younger than 10 years old from African and Asian clinics participating in the International epidemiologic Databases to Evaluate AIDS. The generalized additive model for location, scale, and shape was used to construct normative percentile curves for weight gain at 6, 12, 18, and 24 months following ART initiation. Cox proportional models were used to assess the association between lower percentiles (< 50th) of weight gain distribution at the different time points and subsequent death, virological suppression, and virological failure. Among 7173 children from five regions of the world, 45% were underweight at baseline. Weight gain below the 50th percentile at 6, 12, 18, and 24 months of ART was associated with increased risk of death, independent of baseline characteristics. Poor weight gain was not associated with increased hazards of virological suppression or virological failure. Monitoring weight gain on ART using age-specific and sex-specific normative curves specifically developed for HIV-infected children on ART is a simple, rapid, sustainable tool that can aid in the identification of children who are at increased risk of death in the first year of ART.
    AIDS (London, England) 01/2015; 29(1):101-9.