AIDS reviews (AIDS REV)

Journal description

AIDS Reviews is published quarterly, and covers timely and important topics on the different areas of HIV/AIDS including clinical aspects, therapy, drug resistance, vaccines, virology, evolution, immunology, pathogenesis, diagnostics, epidemiology, opportunistic infections, and prevention.

Current impact factor: 3.79

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 3.787
2013 Impact Factor 4.023
2012 Impact Factor 4.075
2011 Impact Factor 3.512
2010 Impact Factor 4.786
2009 Impact Factor 3.786
2008 Impact Factor 3.268
2007 Impact Factor 3.714
2006 Impact Factor 4.022

Impact factor over time

Impact factor

Additional details

5-year impact 3.59
Cited half-life 5.60
Immediacy index 0.24
Eigenfactor 0.00
Article influence 1.13
Website AIDS Reviews website
ISSN 1139-6121
OCLC 49275522
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Interactions of drugs with renal transporters can reduce the tubular secretion of endogenous products and affect drug pharmacokinetics, efficacy, and toxicity. This review aims to understand the clinical implications of renal transporter-mediated interactions of HIV drugs. These interactions have been fully investigated for nucleoside/nucleotide reverse transcriptase inhibitors, particularly tenofovir disoproxil fumarate, and for some of the newer agents, such as rilpivirine, dolutegravir, and cobicistat. Interactions may include competition, inhibition, or induction of transporters, and interference with renal active secretion of creatinine, the most commonly used marker of renal function. Drug-drug interactions may result in an increased risk of drug toxicity. This interaction is more likely to occur with the protease inhibitors, particularly ritonavir, due to the inhibitory effects of these drugs on specific transporters involved in renal excretion of other drugs. Interactions with the transport of creatinine have been identified with rilpivirine, dolutegravir, and cobicistat. While rilpivirine and dolutegravir inhibit mainly the renal transporter OCT2 in the basolateral membrane of the proximal tubular cell, cobicistat predominantly inhibits the renal transporter MATE1 in the luminal membrane. These interactions can cause mild-to-moderate increases in serum creatinine concentrations and moderate reductions in estimated glomerular filtration rate that do not translate into real decreases in glomerular filtration. To use these drugs safely, clinicians must correctly interpret changes upon initiation of therapy to differentiate these spurious elevations in serum creatinine from clinically significant toxicity. In this article we propose a set of recommendations for clinical use of antiretroviral drugs that interfere with creatinine renal transporters.
    AIDS reviews 10/2014; 16(4).
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    ABSTRACT: An increased prevalence of osteopenia and osteoporosis has been observed in HIV-infected cohorts. We investigated the effect of bisphosphonates on bone mineral density in adults with HIV infection. Outcomes of interest were bone mineral density changes measured by dual-energy X-ray absorptiometry at the lumbar spine, femoral neck, and total hip, and adverse events. Data were pooled using the fixed-effects model. We identified eight randomized controlled trials meeting our inclusion criteria, involving 328 participants. Five trials compared alendronate with placebo or no intervention; in three trials the intervention arm received zoledronate. A significant increase in bone mineral density at the lumbar spine was observed in the bisphosphonate group at 48 weeks (MD: 2.84%; 95% CI: 2.11-3.57) and 96 weeks (MD: 6.76%; 95% CI: 4.98-8.54); analogously, bisphosphonates were associated with an increase in total hip bone mineral density at 48 weeks (MD: 2.12%; 95% CI: 1.43-2.81) and 96 weeks (MD: 3.2%; 95% CI: 1.52-4.88). Bisphosphonates were generally well tolerated; no drug-related withdrawals were reported in the five randomized controlled trials assessing alendronate, whereas two patients out of 104 receiving zoledronate experienced acute-phase reactions. In conclusion, administration of oral and intravenous bisphosphonates was associated with increased bone mineral density at the lumbar spine and total hip over two years in HIV-positive patients. However, none of the included trials were long enough to detect the impact of bisphosphonates on a clinically important outcome such as fracture risk. Larger studies with extended follow-up are warranted.
    AIDS reviews 10/2014; 16(4).
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    ABSTRACT: AIDS emerged in 1981, breaking a period of proud medical progresses in controlling infectious diseases with antimicrobials and vaccines. In an unprecedented way, HIV has attracted much attention for three decades, driving the discovery of new extraordinary molecular diagnostic tools and antiviral drugs. As a result, advances in antiretroviral therapy have made it possible to change HIV infection into a chronic illness. However, the prospects for HIV eradication in the short term are not envisioned for the more than 35 million people worldwide estimated to be living with HIV.
    AIDS reviews 10/2014; 16(4):246-7.
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    ABSTRACT: The eradication of HIV is at this moment one of the greatest challenges in the fight against HIV/AIDS. Despite the prolonged effectiveness of current anti-HIV therapies, capable of keeping patients with undetectable viremia for long periods of time, HIV-infected patients cannot be cured due to the establishment of HIV latent reservoirs. Therefore, several therapeutic strategies are being evaluated to eliminate these viral reservoirs. One of these strategies, termed "shock and kill", aims to attack the latent reservoir by simultaneous treatment with HIV-activating agents to stimulate viral replication in latently infected cells and antiretroviral therapy to block new infections. A number of compounds have been suggested for the shock and kill strategy including histone deacetylase inhibitors (HDACI), histone methyltransferases (HMT), DNA methyltransferase inhibitors (DNMTI), and protein kinase C (PKC) activators.
    AIDS reviews 10/2014; 16(4):246.
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    ABSTRACT: The annual workshop of the Spanish HIV‑2/HTLV Study Group was held at the Instituto de Salud Carlos III in Madrid on December 11, 2013. Nearly 100 experts and researchers in retroviruses other than HIV‑1, the classical AIDS agent, convened for a one‑day meeting devoted to updating knowledge on the epidemiology of HIV‑2 and HTLV-1 infections and discussing new diagnostic and therapeutic strategies, with special attention to non‑endemic regions such as Spain. The Group was funded 25 years ago and since then has been responsible for the national registry of cases, recording all relevant information for each subject and inviting them to enroll in a prospective cohort and biobank. Up to the end of 2013, a total of 297 individuals with HIV‑2 infection were reported in Spain. All but 10 carry HIV‑2 subtype A, with the rest being infected with subtype B. Overall, 71% came from sub‑Saharan Africa. During the last decade, the incidence of new HIV‑2 infections in Spain has remained fairly stable with around 20 cases per year. At the time of diagnosis, plasma HIV‑2 RNA was undetectable in 61% of individuals and values in viremic subjects tended to be low (2.8 logs on average). To date, only 26% of HIV‑2 individuals have been treated with antiretrovirals. The CD4 counts, however, only increased above 200 cells/mm³ in 42% of them. On the other hand, 74% of non‑treated HIV‑2 individuals have > 500 CD4+ T‑cells/mm³. As in HIV‑1 infection, X4 tropism in HIV‑2 is associated with lower CD4 counts. A total of 253 individuals with HTLV-1 infection were reported in Spain by the end of 2013. Overall, 58% came from Latin America. HTLV-1‑associated myelopathy was diagnosed in 29 patients and adult T‑cell leukemia/lymphoma in 18. The highest incidence occurred in 2013, with 34 new HTLV-1 diagnoses, largely as result of expanding HTLV screening in blood banks. Attempts to reduce HTLV-1 proviral load in symptomatic or asymptomatic patients with elevated HTLV-1 DNA using antiretrovirals have produced poor results, although integrase inhibitors could be more successful. Although no cases of HTLV‑3 or ‑4 have been identified so far in Spain, 769 individuals have been diagnosed with HTLV‑2 infection. Up to 85% of the latest cases are coinfected with HIV‑1 and are former intravenous drug users.
    AIDS reviews 09/2014; 16(3).
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    ABSTRACT: When AIDS was first recognized in 1981 and HIV was discovered as its cause in 1983, we could never have imagined the rapid worldwide expansion of the pandemic. Neither could we have expected the great success of antiretroviral therapy. Nevertheless, in contrast with the hepatitis C virus (HCV), another RNA virus that affects large patient populations and for which new drugs promise a cure, HIV cannot be eradicated with only antiviral treatment.
    AIDS reviews 07/2014; 16(3):183.
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    ABSTRACT: World Health Organization-recommended surveys of acquired HIV-1 drug resistance include assessment of HIV-1 viral load suppression to levels below 1,000 copies/ml and drug resistance-associated mutation patterns in subjects on antiretroviral therapy. Surveys are being conducted in regions of the world that cannot support the collection, storage, and shipping of frozen plasma. Therefore, dried blood spots are often the specimen type of choice for both genotyping and viral load measurement. Furthermore, viral load testing for individual patient management in these regions is being scaled-up in accordance with WHO 2013 Guidelines for Antiretroviral Treatment. Technical issues related to the adaptation of viral load assays to dried blood spots, especially with respect to sensitivity (limit of detection), specificity (cell-free RNA vs. cell-associated DNA or RNA), and assay method, affect the interpretation of a viral load result from dried blood spots. Amongst published studies of commercial assay performance with dried blood spots, the bioMérieux EasyQ® and Abbott RealTime assays tended to show high (> 90%) specificity and sensitivity; the Biocentric Generic or Roche TaqMan® assays tended to show high sensitivity but lower specificity, using a 1,000 copies/ml threshold. The relative contribution of cell-associated DNA or RNA to a viral load measurement is likely to vary between patients, depending on clinical parameters and treatment status. A model was developed that predicts that in patients on antiretroviral therapy with low plasma viral load, cellular DNA is the predominant source of non-plasma virus-derived nucleic acid in dried blood spots. The extent of viral load overestimation from dried blood spots becomes less important when plasma viral load is over about 5,000 copies/ml. To avoid misclassifying subjects with plasma viral load suppression, the World Health Organization-recommended threshold of 1,000 copies/ml can be applied only when an assay that can distinguish between DNA and RNA is used (e.g. bioMérieux EasyQ® or Abbott RealTime). There is a need for additional affordable technologies with the ability to discriminate between cell-free (plasma) and cell-associated nucleic acids.
    AIDS reviews 07/2014; 16(3):160-171.
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    ABSTRACT: The 2014 International Antiviral Society (IAS) Conference was held in Melbourne, Australia in July. This major HIV/AIDS scientific event was accompanied by the publication of several pivotal studies in the field in different medical journals. We discuss below some of the most important implications derived from these new releases.
    AIDS reviews 07/2014; 16(3):182-183.
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    ABSTRACT: The U.S. Department of Health and Human Services (DHHS) released on May 1st an update of its Guidelines for the Use of Antiretroviral Agents in HIV-1-Infected Adults and Adolescents ( Among the major changes is the addition of a new section on cost considerations and a recommendation for less frequent CD4+ T-cell monitoring for people without advanced disease.
    AIDS reviews 04/2014; 16(2):117-8.
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    ABSTRACT: In May 2014, the US Centers for Disease Control and Prevention (CDC) issued new recommendations for the prescription of Truvada® as pre-exposure prophylaxis (PrEP) for persons engaged in high-risk HIV behaviors, be they homosexuals, heterosexuals, or injecting drug users (
    AIDS reviews 04/2014; 16(2):118-9.

  • AIDS reviews 01/2013; 15:139-145.
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    ABSTRACT: We surveyed current trends in epigenetics in general and epigenetics of HIV infection and AIDS in particular to pinpoint promising areas for translational research. Epigenetic mechanisms mark and affect the structure of chromatin, thereby controlling the activity of promoters. Because epigenetic changes are reversible, epigenetic drugs can be used to modulate gene activity. At present, silenced HIV genomes, the latent HIV reservoir, is a major obstacle for a curative treatment of AIDS patients. Epigenetic therapy aims at the purging of the latent reservoir by switching on transcription of silent HIV genomes. The basic idea is that the cytopathic effect of the replicating virus and the immune system may eliminate the reactivated cells, whereas HAART may block the infection of new target cells. Although current efforts concentrate on long-lived resting memory CD4+ T-cells, dormant HIV proviruses also reside in other cell types. Thus, epigenetic characterization of the various HIV-infected host cells and host cell-dependent HIV latency mechanisms is a promising research area and may facilitate the development of cell type-specific epigenetic drugs. HAART itself affects the epigenotype of host cells. This may contribute to the development of drug resistance and unwanted side effects. A pharmacoepigenetic approach may help to elucidate and revert such phenomena. In addition to latent reservoir purging, epigenetic research offers alternative therapeutic tools as well; although not aimed at the elimination of the virus, targeted silencing of HIV transcription by epigenetic regulators may help HAART to minimize virus replication.
    AIDS reviews 01/2013; 15:181-188.
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    ABSTRACT: The oldest pandemic HIV-1 (group M) sequence known was, up to recently, the ZR59, isolated from an adult male from Kinshasa, Democratic Republic of Congo (DRC), in 1959 (Zhu, et al. Nature. 1998;391:594-7). This sequence branches from within the subtype D lineage after the latter splits from B. The genetic distance between ZR59 and the M-root is about half of that of modern sequences. This fact alone suggested that the MRCA existed decades prior to 1959, in line with molecular clock dating studies which placed it around 1920-1930 (e.g. Salemi, et al. FASEB J. 2001;15:276-8; Korber, et al. Science. 2000;288:1789-96). In October 2008, Worobey, et al. (Nature 2008;455:661-5) reported the analysis of a new partial sequence isolated from paraffin-embedded lymph nodes of a woman from Kinshasa, collected and stored in 1960. The sequence, which they designated "DRC60", clusters with subtype A and, like ZR59, is much closer to the root than modern strains. For a small env region, both DRC60 and ZR59 fragments are available. So now we have two sequences which argue for an origin of pandemic HIV-1 decades before 1960. The authors re-estimated the MRCA timing, applying a relaxed clock coalescent framework. Without the ZR59 and DRC60 sequences included, they obtained a time around 1930, as in previous studies, but when they included these two strains, which provided early calibration points, and therefore improved the reliability of the estimates, the best-fit results, and their 95% CI, became 1921 (1908-33) under a constant population size model, 1902 (1873-1922) under an expansion model, and 1908 (1884-1924) under a Bayesian skyline plot model. The new study suggests that HIV-1-M has been around for longer than previously thought. An origin in the period 1930-35 is now less likely, occupying the upper end of the probability distribution, in one of the models only. The fact that the two donors of ZR59 and DRC60 were opposite-sex adults may suggest that the epidemic was already predominantly heterosexual by that time. The clustering of these strains with different subtypes suggests that in Kinshasa, by 1960, a wide genetic variation of HIV-1-M already existed, and this broadly reinforces the view that this city was the epicenter for HIV-1-M emergence and spreading. It is unknown if viral adaptation was necessary for epidemic emergence, and if it was, what process drove it. Some proposed parenteral serial transmission as the key factor (Drucker, et al. Lancet. 2001;358:1989-92), while others suggested urbanization and social changes. These theories leave several loose ends unexplained. One is that the dating of all epidemic HIV groups (HIV-1 groups M and O, and HIV-2 groups A and B) point to early 20th century, and injection intensity peaked after mid-20th century, therefore raising the question of why no more groups emerged after mid-20th century if injections were the key factor. Such potential new groups would have had time to spread enough to be noticed (Lemey, et al. PNAS. 2003;100:6588-92; Lemey, et al. Genetics. 2004;167:1059-68). Cities also grew exponentially, attracted many more potentially SIV-infected rural migrants after the mid century, raising the same question. The existing theories also fail to explain the biogeography of epidemic HIV groups, and why they are so few, despite bushmeat-related human SIV infections being not uncommon (Kalish, et al. Emerg Inf Dis. 2005;11:1928-30), and injections, urbanization, and migration, so ubiquitous. Thus, the enigma about the origin of HIV is still not solved, but with more data on early HIV emerging, we are coming closer to a general picture of the circumstances that permitted it.
    AIDS reviews 01/2009; 11(1):52.
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    ABSTRACT: Castleman's disease is characterized by a non-clonal lymph node hyperplasia. Pathologically it is classified as hyaline vascular, plasmacytic, or mixed cellularity types, and clinically it may adopt a unicentric (localized) or multicentric presentation. An association of the disease with HIV infection has been found. Many uncertainties remain concerning the etiopathogenesis and the optimal treatment of this rare condition.
    AIDS reviews 01/2009; 11(1):3-7.