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

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
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    • 12 months embargo
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    • Must include statement that it is not the final published version
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    • 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)
    • Publisher last reviewed on 19/03/2015
  • Classification
    ​ yellow

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: We investigated kidney function outcome in 24 chronic hepatitis C genotype 1 patients coinfected with HIV receiving telaprevir in a single tertiary care hospital in Spain. A statistically significant median (interquartile range) decrease in estimated glomerular filtration rate (eGFR, ml/min/1.73 m) relative to baseline [93.6 (73.0-109.0)] was seen at weeks 4 [86.5 (34.0-112.0), P = 0.014], 8 [90.0 (49.0-111.0), P = 0.026] and 12 [89.5 (54.0-113.0), P = 0.017]. These changes reversed after telaprevir discontinuation. Patients presenting an eGFR decrease had a higher risk of haematological toxicity.
    AIDS (London, England) 03/2015; DOI:10.1097/QAD.0000000000000643
  • AIDS (London, England) 03/2015; 29(5):641-2. DOI:10.1097/QAD.0000000000000566
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    ABSTRACT: We explored the impact of lifelong cumulative HIV viremia on immunological recovery during antiretroviral therapy, according to the timing of treatment initiation. We estimated lifelong cumulative HIV viremia in patients followed in the ANRS PRIMO cohort since primary infection, including 244 patients who started treatment during PHI and had at least one treatment interruption, and 218 patients who started treatment later but with no interruptions. The impact of cumulative viremia on current immunological status was analysed using linear and logistic regression models. At the last visit on treatment, median CD4 cell count was 645 cells/μl in the early/intermittent treatment group (median time from infection 9.5 years, 4.8 years of continuous treatment since last resumption), and 654 cells/μl in the deferred/continuous treatment group (median time from infection 6.1 years, 3.0 years of continuous treatment). Only 36.1 and 39.8% of patients achieved a CD4/CD8 ratio of more than 1, respectively. Current CD4 cell count was not associated with cumulative HIV viremia in either group. In contrast, patients with high cumulative HIV viremia (>66th percentile vs. <33rd percentile) were less likely to achieve a CD4/CD8 ratio of more than 1 (26.8 vs. 43.3%, P = 0.003), even after controlling for the baseline CD4/CD8 ratio, treatment duration, sex and age. Much higher CD4 cell count and CD4/CD8 ratio were reached in early/continuous treatment, that is low viremia exposure group. Our results underline the critical need in early-treated patients to maintain adherence, in order to limit cumulative HIV viremia and optimize immunological recovery, notably the CD4/CD8 ratio.
    AIDS (London, England) 03/2015; 29(5):595-607. DOI:10.1097/QAD.0000000000000571
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    ABSTRACT: HIV genetic diversity is a major obstacle for vaccine development. To define whether potential T-cell epitope (PTE) peptide usage improves the detection of T cell responses in a highly diverse HIV-1 epidemic, we compared the magnitude, breadth and depth of group M PTE peptide responses to consensus M peptides in Gag and Nef proteins. Gag PTE responses were detected at a higher magnitude, more Nef PTE responses were detected at a cohort (but not individual) level and depth was detected in both Gag and Nef responses.
    AIDS (London, England) 03/2015; 29(5):635-9. DOI:10.1097/QAD.0000000000000581
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    ABSTRACT: The objective of this study is to identify human leukocyte antigen (HLA) class I and killer-cell immunoglobulin-like receptor (KIR) genotypes associated with different risks for HIV acquisition and HIV disease progression. A cross-sectional study of a cohort of 468 high-risk individuals (246 HIV-positive and 222 HIV-negative) from outpatient clinics in Lima (Perú). The cohort was high-resolution HLA and KIR-typed and analysed for potential differences in single-allele frequencies and allele combinations between HIV-positive and HIV-negative individuals and for associations with HIV viral load and CD4 cell counts in infected individuals. HLA class I alleles associated with a lack of viral control had a significantly higher population frequency than relatively protective alleles (P = 0.0093), in line with a rare allele advantage. HLA-A02 : 01 and HLA-C04 : 01 were both associated with high viral loads (P = 0.0313 and 0.0001, respectively) and low CD4 cell counts (P = 0.0008 and 0.0087, respectively). Importantly, the association between HLA-C04 : 01 and poor viral control was not due to its linkage disequilibrium with other HLA alleles. Rather, the coexpression of its putative KIR ligand KIR2DS4f was critically linked to elevated viral loads. These results highlight the impact of population allele frequency on viral control and identify a novel association between HLA-C04 : 01 in combination with KIR2DS4f and uncontrolled HIV infection. Our data further support the importance of the interplay of markers of the adaptive and innate immune system in viral control.
    AIDS (London, England) 03/2015; 29(5):507-17. DOI:10.1097/QAD.0000000000000574
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    ABSTRACT: Injecting drug use has historically been the principal driver of the HIV epidemic in the northeast states of India. However, recent data indicate growing numbers of people who inject drugs (PWIDs) in north and central Indian cities. We conducted face-to-face surveys among PWIDs in seven northeast and eight north/central Indian cities using respondent-driven sampling. We used a rapid HIV-testing protocol to identify seropositive individuals and multiassay algorithm to identify those with recent infection. We used multilevel regression models that incorporated sampling weights and had random intercepts for site to assess risk factors for prevalent and incident (recent) HIV infection. We surveyed 14 481 PWIDs from 15 Indian cities between January and December 2013. Participants reported high rates of needle/syringe sharing. The median (site range) estimated HIV prevalence and incidence were 18.1% (5.9, 44.9) and 2.9 per 100 person-years (0, 12.4), respectively. HIV prevalence was higher in northeast sites, whereas HIV incidence was higher in north/central sites. The odds of prevalent HIV were over three-fold higher in women than in men. Other factors associated with HIV prevalence or incidence included duration since first injection, injection of pharmaceutical drugs, and needle/syringe sharing. The burden of HIV infection is high among PWIDs in India, and may be increasing in cities where injecting drug use is emerging. Women who inject drugs were at substantially higher risk for HIV than men - a situation that may be mediated by dual injection-related and sexual risks.
    AIDS (London, England) 03/2015; 29(5):619-28. DOI:10.1097/QAD.0000000000000592
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    ABSTRACT: Understanding the role of T-cell immunoglobulin and mucin domain-containing molecule 3 (Tim-3) on T cells and dendritic cells during the course of simian immunodeficiency virus (SIV) infection. Sequentially collected PBMCs from uninfected and SIVmac239-infected rhesus macaques were evaluated for Tim-3 expression by flow cytometry and antigen-specific responses. Blood innate immune cells (dendritic cells) and B cells showed high constitutive expression of Tim-3, whereas, compared to humans, only a minority of macaque T cells did. However, TIM-3 expression was transiently up-regulated on both CD4 and CD8 T cells during acute SIV infection, correlating with plasma viral loads, CD4 cell counts, and Ki67 expression up to 6 weeks postinfection and returned to baseline values by 8 weeks postinfection. Upon antigen-specific stimulation, most Tim-3 T cells produced various cytokines, suggesting that this marker is up-regulated on effector antigen-specific T cells and not associated with T-cell exhaustion. Among myeloid dendritic cells (mDCs), a clear separation was seen between blood mDCs expressing Tim-3 and those expressing PD-L2 - a ligand for inhibitory receptor programmed death 1. Rhesus macaques show constitutive expression of Tim-3 primarily on innate immune cells, but markedly lower levels on T cells compared to humans. Nevertheless, Tim-3 expression on T cells is transiently up-regulated during acute, but not chronic, SIV infection, and appears to be a marker of antigen-specific effector cells. The exact role and contribution of Tim-3 to the modulation of antiviral responses in vivo will require additional investigation.
    AIDS (London, England) 03/2015; 29(5):531-6. DOI:10.1097/QAD.0000000000000589
  • AIDS (London, England) 03/2015; 29(5):629-31. DOI:10.1097/QAD.0000000000000593
  • AIDS (London, England) 03/2015; 29(5):643-5. DOI:10.1097/QAD.0000000000000577
  • AIDS (London, England) 03/2015; 29(5):642-3. DOI:10.1097/QAD.0000000000000567
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    ABSTRACT: We examined HIV transmission potential of patients in care by analyzing the amount of person-time spent above a viral load threshold that increases risk for transmission. Observational cohort and supplemental data. The cohort included HIV patients who received care at six HIV clinics in the United States, from 1 April 2009 to 31 March 2013, and had two or more viral load tests during this interval. Person-time (in days) above a viral load of 1500 copies/ml out of the total observation time was determined by inspecting consecutive pairs of viral load results and the time intervals between those pairs. The person-time rate ratios comparing demographic and clinical subgroups were estimated with Poisson regression. The cohort included 14 532 patients observed for a median of 1073 days with a median of 9 viral load records. Ninety per cent of the patients had been prescribed antiretroviral therapy. On average, viral load exceeded 1500 copies/ml during 23% of the patients' observation time (average of 84 days per year, per patient). Percentage of person-time above the threshold was higher among patients who had more than a fourth of their viral load pairs exceeding a 6-month interval (34% of observation time), patients not on antiretroviral therapy (58% of time), new/re-engaging patients (34% of time), patients 16-39 years of age (32% of time), and patients of black race (26% of time). HIV patients in care spent an average of nearly a quarter of their time with viral loads above 1500 copies/ml, higher among some subgroups, placing them at risk for potentially transmitting HIV to others.
    AIDS (London, England) 03/2015; DOI:10.1097/QAD.0000000000000640
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    ABSTRACT: Latent HIV type I (HIV-1) infections can frequently occur in short-lived proliferating effector T-lymphocytes. These latently infected cells could revert into resting T-lymphocytes and thereby contribute to the establishment of the long-lived viral reservoir. Monocyte-derived dendritic cells can revert latency in effector T-cells in vitro. Here we investigated the latency activation properties of tissue-specific immune cells, including a large panel of dendritic cell subsets, to explore in which body compartments effector T-cells are most likely to maintain latent HIV-1 provirus and thus potentially contribute to the long-lived reservoir. Our results demonstrate that blood or genital tract dendritic cells do not activate latent provirus in effector T-cells, whereas gut or lymphoid dendritic cells induce virus production from latently infected effector T-cells in our in-vitro model for latency. Toll-like receptor 3-induced interferon production by myeloid dendritic cells abolished the dendritic cells' ability to induce viral gene expression. In this study, we show that HIV-1 provirus residing in the effector T-cells is activated from latency by tissue-specific dendritic cell subsets and other immune cells with remarkably different efficiencies.Our new assay system points to an important, neglected aspect of HIV-1 research: the ability of other immune cells, especially dendritic cells, to differentially affect latency establishment as well as virus reactivation.
    AIDS (London, England) 03/2015; DOI:10.1097/QAD.0000000000000637
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    ABSTRACT: Tenofovir disoproxil fumarate (TDF) nephrotoxicity is characterized by proximal renal tubular injury and dysmorphic mitochondria resulting in proteinuria, orthoglycemic glycosuria, and other markers of proximal tubular dysfunction. The objective of this study was to determine the pattern of proteinuria in patients with biopsy-proven TDF nephrotoxicity. Retrospective chart review METHODS:: Patients with biopsy-proven TDF nephrotoxicity were identified and their medical charts and biopsy reports were reviewed. Comparison was made with HIV-infected patients not on TDF who underwent kidney biopsy. We identified 43 biopsy-proven cases of TDF nephrotoxicity; mean age 54.7 ± 0.4 years, 53% men, 42% whites. Thirty-seven cases reported proteinuria by dipstick of which only 60% had at least 2+ proteinuria. Twenty-seven patients had urine protein quantified by either 24-h collection or spot urine protein-to-creatinine ratio; median proteinuria was 1742 mg/day [interquartile range (IQR) 1200-2000 mg] and 1667 mg/g creatinine (IQR 851-1967 mg/g), respectively. Ten patients had concurrent urinary albumin measured, with a median 236 mg/g creatinine (IQR 137-343 mg/g). The mean urine albumin-to-urine protein ratio (uAPR) was 0.17 (IQR 0.14-0.19), confirming that TDF nephrotoxicity is primarily associated with nonalbumin proteinuria. Control cases had a uAPR of 0.65 (IQR 0.55-0.79) P < 0.001. Histopathology showed the predominance of proximal tubular injury with characteristic mitochondrial abnormalities. In the largest published cohort of patients with biopsy-proven TDF nephrotoxicity, we show that low uAPR is a reliable feature of this disease. Because of the predominance of nonalbumin proteinuria, dipstick urinalysis may be unreliable in TDF nephrotoxicity.
    AIDS (London, England) 03/2015; DOI:10.1097/QAD.0000000000000628
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    ABSTRACT: Risk-benefit assessment of combination antiretroviral therapy (cART) requires consideration of all potential serious harms. Studies of initial cART may permit identification of associations between particular regimens and uncommon harms, but only if comprehensively reported in the public domain. Study-based, systematic review of published initial cART studies (in adult patients) for the completeness of serious harms reporting. Electronic databases, abstracts, and regulatory/sponsor reports were searched (1 January 1996 - 31 December 2012). Reporting of pre-specified harms - deaths, new/recurrent AIDS events, serious non-AIDS events (2010 INSIGHT classification) and serious adverse events (SAEs) - were assessed as the proportion of studies providing data (reporting frequency). Pharmaceutical sponsors were approached for unreported data. 103 studies (86% randomized, 54% industry-sponsored) were included. Deaths, AIDS events, serious non-AIDS events and SAEs were reported for 85 (83%), 55 (53%), 26 (25%) and 43 (42%) studies, respectively. Deaths were better reported for academic than industry-sponsored studies (91 vs. 75%; P = 0.03); the converse applied for SAEs (26 vs. 55%; P = 0.002). SAEs were better reported for randomized than cohort studies (46 vs. 14%; P = 0.03), and for phase 3 than phase 2 or 4 studies (58 vs. 32 and 29%, respectively; P = 0.02). SAE reporting increased over time [ρ = 0.704, P = 0.002 (Spearman)]. Unreported data acquired for 34 (61%) of 56 industry-sponsored studies improved ascertainment in these studies to be between 82 and 100% (P < 0.001). Public domain reporting of serious harms for initial cART studies is limited. Insufficient data exist to determine if particular ART drugs/regimens are associated with most serious harms.
    AIDS (London, England) 03/2015; DOI:10.1097/QAD.0000000000000633
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    ABSTRACT: The HLA-A*30-B*13-C*06 haplotype is reported to be associated with slow disease progression in HIV-1-infected Northern Han Chinese, but the mechanism remains unknown. Gag-specific T cell responses and gag sequencing were performed in nine B' clade HIV-1-infected HLA-A*30-B*13-C*06-positive slow progressors to understand HLA associated viral control. IFN-γ ELISPOT assays were performed to determine the Gag-specific T cell responses and cross reactivity to variants peptides. Longitudinal HIV-1 gag sequencing was performed at clonal level. The overlapping peptides (OLP)-48: RQANFLGKIWPSHKGRPGNF (RL42 Gag434-453); OLP-2: GQLDRWEKIRLRPGGKKKYR (RL42 Gag11-30); OLP-15: VQNLQGQMVHQPISPRTLNA (RL42 Gag135-154) and OLP-16: HQPISPRTLNAWVKVVEEKA (RL42 Gag144-163) were dominant in HLA-A*30-B*13-C*06-positive patients. A new epitope (HQPISPRTL (Gag144-152, HL9)) within OLP-15 and OLP-16 was identified. Results showed that strong cross reactive responses to multiple immunodominant peptides were associated with better clinical outcomes. In addition, efficient cross-recognition of HL9 autologous variants developed in patients was associated with high CD4 T-cell counts. However, two patients who had developed mutations to their dominant responses during the follow up experienced decrease in CD4 T-cell counts. It appears that Gag-specific T cell responses against one or more un-mutated epitopes or cross-recognition of autologous epitope variants contribute to slow disease progression in HLA-A*30-B*13-C*06-positive patients. We conclude that a single "appropriate" Gag-specific T cell response appears to be sufficient to protect patients from disease progression. HLA-A*30-B*13-C*06-positive individuals benefited from having a choice of numerous immunodominant gag epitopes for T cells to react. The study offers new insight for future design of T cell based HIV-1 vaccine.
    AIDS (London, England) 03/2015; DOI:10.1097/QAD.0000000000000652
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    ABSTRACT: CODOX-M/IVAC chemotherapy is commonly used to treat Burkitt lymphoma and in the HIV-negative population. Rituximab is often added with suggested survival benefits. Concerns over increased toxicity in an already immunocompromized population have prevented its routine addition in people living with HIV (PLWH). This study evaluated the effect on treatment-related toxicity and efficacy of adding rituximab to CODOX-M/IVAC chemotherapy in PLWH. Retrospective review of 91 PLWH (74 men) with Burkitt lymphoma treated in five London centers between 2003 and 2013. All patients received combination antiretroviral therapy. Forty-nine patients received CODOX-M/IVAC and 42 R-CODOX-M/R-IVAC. The addition of rituximab did not confer any significant increase in grade 3/4 toxicities including infections, mucositis, diarrhea, renal impairment, and tumor lysis syndrome. There was no significant difference in toxic deaths between groups (P = 0.14). The 2-year overall survival (OS) was greater for patients receiving rituximab {2-year OS 72% [95% confidence interval (CI) 0.22-0.92, hazard ratio 0.46] vs. 55% [95% CI 1.1-4.5, hazard ratio 2.2]; log-rank P = 0.04}. Similarly, the 2-year progression-free survival (PFS) was greater in the rituximab cohort [2-year PFS 81% (95% CI 0.21-0.99, hazard ratio 0.46) vs. 55% (95% CI 1.0-4.8, hazard ratio 2.2); log-rank P = 0.04]. Our multicenter analysis is the largest to date in this population and showed that the addition of rituximab to CODOX-M/IVAC chemotherapy confers no increase in toxicity and results in significantly improved OS and PFS in PLWH with Burkitt lymphoma who receive concomitant combination antiretroviral therapy.
    AIDS (London, England) 02/2015; DOI:10.1097/QAD.0000000000000623
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    ABSTRACT: To determine viral and immune factors involved in transmission and control of HIV-1 infection in persons without functional CCR5. Understanding transmission and control of HIV-1 in persons homozygous for CCR5 is important given efforts to develop HIV-1 curative therapies aimed at modifying or disrupting CCR5 expression. We identified two HIV-infected CCR5 individuals among a cohort of patients with spontaneous control of HIV-1 infection without antiretroviral therapy and determined coreceptor usage of the infecting viruses. We assessed genetic evolution of full-length HIV-1 envelope sequences by single-genome analysis from one participant and his sexual partner, and explored HIV-1 immune responses and HIV-1 mutations following virologic escape and disease progression. Both participants experienced viremia of less than 4000 RNA copies/ml with preserved CD4 T-cell counts off antiretroviral therapy for at least 3.3 and 4.6 years after diagnosis, respectively. One participant had phenotypic evidence of X4 virus, had no known favorable human leukocyte antigen alleles, and appeared to be infected by minority X4 virus from a pool that predominately used CCR5 for entry. The second participant had virus that was unable to use CXCR4 for entry in phenotypic assay but was able to engage alternative viral coreceptors (e.g., CXCR6) in vitro. Our study demonstrates that individuals may be infected by minority X4 viruses from a population that predominately uses CCR5 for entry, and that viruses may bypass traditional HIV-1 coreceptors (CCR5 and CXCR4) completely by engaging alternative coreceptors to establish and propagate HIV-1 infection.
    AIDS (London, England) 02/2015; DOI:10.1097/QAD.0000000000000629