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The main route of human immunodeficiency virus (HIV) infection in children is from mother to child. The preventive measures established for the Aids Clinical Trial Group protocol 076 (ACTG 076) significantly reduces HIV vertical transmission rates. This study aims to evaluate the implementation of the ACTG 076 protocol in the maternity units of State of Sergipe, Brazilian northeast.
To compare the effect of two dose regimens of zidovudine in the treatment of severe HIV-related thrombocytopenia (TP).
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Randomised trials comparing any intervention aimed at decreasing the risk of mother-to-child transmission of HIV infection compared with placebo or no treatment, or any two or more interventions aimed at decreasing the risk of mother-to-child transmission of HIV infection.
HIV/AIDS patients on HAART could be at a greater risk of having DM than HAART-naïve patients as a result of the effect of HAART on risk factors of DM such as BMI and blood pressure.
The median follow-up to date of death or last known vital status was 43 months (10th percentile 18 months; 90th percentile 55 months). The proportion of participants remaining on their allocated treatment fell steadily over time; by 4 years after trial entry, 3% remained on ZDV, 20% on ZDV + ddI and 21% on ZDV + ddC. Changes mainly involved the stopping, addition or switching of a nucleoside reverse transcriptase inhibitor (NRTIs). There was little use of protease inhibitors (PIs) or non-nucleoside reverse transcriptase inhibitors (NNRTIs) before the third year of the trial. Between the third and fourth years, regimens included a drug from one of these classes for approximately 17% of person-time in all treatment groups. Relative to ZDV monotherapy, the beneficial effects of combination therapy on mortality and disease progression rates increased significantly with time since randomization. The maximum effects on mortality were observed between 2 and 3 years, with a 48% reduction for ZDV + ddI and a 26% reduction for ZDV + ddC. These rates were observed when the original allocated treatment was received 42% and 47% of the time in the ZDV + ddI and ZDV + ddC groups, respectively. The mean CD4 count remained significantly higher (approximately 50 cells/microL) in the combination therapy groups 4 years after randomization, suggesting a projection of a clinical benefit beyond this time point.
Progressive left ventricular dilatation occurred in children with symptomatic HIV infection. Compensatory hypertrophy also occurred but was inadequate to maintain peak systolic wall stress within the normal range. The progressive elevation of ventricular afterload due to dilatation resulted in depressed ventricular performance, but intrinsic ventricular contractility remained normal. Zidovudine did not appear to worsen or ameliorate these cardiac changes.
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HAART induced a significant increase in the PLT count (chi(2)=10.53, P=0.01) within the third month which was sustained up to the sixth month of therapy. No STP relapse was observed among eight PLT responders followed for longer than 6 months (median 27; range 7-41 months). The PLT increase after HAART was similar to that observed with AZT monotherapy, but a greater number of HAART patients were antiretroviral-experienced. HAART determined a PLT response in 10/13 subjects whose thrombocytopenia had not improved after previous AZT monotherapy. After 6 months of HAART, a complete platelet response occurred more frequently in patients with undetectable plasma HIV-RNA levels (P=0.01).
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L-696,229 (3-[2-(benzoxazol-2-yl)ethyl]-5-ethyl-6-methyl-pyridin-2 (1H)-one) is a specific inhibitor of human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT) activity that possesses antiviral activity in cell culture (W.S. Saari, J.M. Hoffman, J.S. Wai, T.E. Fisher, C.S. Rooney, A.M. Smith, C.M. Thomas, M. E. Goldman, J. A. O'Brien, J. H. Nunberg, J. C. Quintero, W. A. Schleif, E. A. Emini, and P. S. Anderson, J. Med. Chem. 34:2922-2925, 1991). In the present study, the RT-inhibitory activity and antiviral properties were characterized in detail. The inhibition of RT activity was template-primer dependent with 50% inhibitory concentrations of 0.018 to 0.50 microM and was noncompetitive with respect to deoxynucleoside triphosphates. L-696,229 inhibited RT activity in a mutually exclusive manner with respect to either phosphonoformate or azidothymidine triphosphate and was a weak partial inhibitor of the RNase H activity associated with HIV-1 RT. The compound did not significantly inhibit other retroviral or cellular polymerases at 300 microM.L-696,229 inhibited the spread of HIV-1 infection in cell cultures with all cell types and viral isolates tested, including human peripheral blood mononuclear cells and a virus isolate resistant to azidothymidine.
Trizivir was clinically equivalent to Combivir-ABC and may be substituted for the latter to simplify treatment and reduce pill burden.
To investigate the evidence for the existence of gender bias (defined as care provided independently of clinical need) in the use of specialist services by critically appraising the literature.
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The STI of HAART in cycles of 4 weeks off/12 weeks on therapy in children with chronically undetectable VL can cause progressively lower viral rebounds followed by a decrease to undetectable levels, with a low risk of severe immunosuppression and without the occurrence of symptoms related to HIV.
In June 2001 the United Nations Special Assembly on HIV/AIDS set reduction targets of 20% and 50% for the numbers of children newly infected with HIV by 2005 and 2010 respectively. Are these targets achievable? Antiretroviral monotherapy during pregnancy, delivery, and the neonatal period can reduce the rate of mother-to-child transmission of HIV-1 by two-thirds in non-breastfeeding populations. Shorter and simpler regimens of monotherapy have been associated with a reduction of 50% in such transmission among non-breastfeeding populations and of up to 40% in breastfeeding populations. Delivery by elective caesarean section is associated with a halving of the risk of mother-to-child transmission. However, breastfeeding poses a substantial additional risk of acquisition of HIV, and if prolonged it more than doubles the overall rate of transmission. Rates below 2% are being reported from settings where combination therapy is applied during pregnancy and delivery, delivery is by elective caesarean section, and breastfeeding does not take place. In breastfeeding populations where elective caesarean delivery is not an option but peripartum antiretroviral therapy is used, rates at six weeks are about 10% but can be 25% or more after 18 months of breastfeeding. More widely applicable interventions are being developed, such as cleansing of the birth canal and antiretroviral therapy during the breastfeeding period.
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This retrospective cohort study utilized clinical data of HIV-1 infected adults (aged ≥15 years), commenced on efavirenz containing-regimen between January 2004 and December 2011. The time-dependent occurrence of clinical adverse events as defined by the World Health Organization was analyzed by Cox regression analysis.
This systematic review focuses on antiretroviral therapy (ART) for treating human immunodeficiency virus (HIV) infection in ART-eligible pregnant women. Mother-to-child transmission (MTCT) is the primary means by which children worldwide acquire HIV infection. MTCT occurs during three major timepoints during pregnancy and the postpartum period: in utero, intrapartum, and during breastfeeding. Strategies to reduce MTCT focus on these periods of exposure and include maternal and infant use of ART, caesarean section before onset of labour or rupture of membranes, and complete avoidance of breastfeeding. Where these combined interventions are available, the risk of MTCT is as low as 1-2%. Thus, ART used among mothers who require treatment of HIV for their own health also plays a significant role in decreasing MTCT.This review is one in a series of systematic reviews performed in preparation for the revision of the 2006 World Health Organization (WHO) Guidelines regarding "Antiretroviral Drugs for Treating Pregnant Women and Preventing HIV Infection in Infants" and "Antiretroviral therapy (ART) for HIV Infections in Adults and Adolescents." The findings from these reviews were discussed with experts, key stakeholders, and country representatives at the 2009 WHO guideline review meeting. The resulting WHO 2009 "rapid advice" preliminary guidance on adult and adolescent ART now recommends lifelong treatment for all adults with HIV infection and CD4 counts <350 cells/mm(3). These recommendations also apply to pregnant women who are HIV-infected and they place a high value on early ART to benefit the mother's own health (WHO 2009). The "rapid advice" preliminary guidance also aims to minimize side effects for mothers and their infants (WHO 2009).
Median baseline values for all subjects were 42 420 copies/ml for HIV RNA and 277 x 10(6)/l for CD4 count. During the trial a significantly lower HIV RNA level and higher CD4 count was sustained in the ZDV/3TC group compared with the other group, with a difference in the median area under the curve from baseline per month of follow-up of 0.38 log10 copies/ml HIV RNA and 0.18 log2 x 10(6)/l CD4 cells (P < 0.001 in each case). For patients who were initially asymptomatic or in CDC stage B, the adjusted relative hazard (RH) of AIDS for a twofold lower CD4 count was 3.14 [95% confidence interval (CI), 1.44-6.83] and for a 10-fold higher HIV RNA level was 3.22 (1.20-8.59). The RH progression to AIDS expected with ZDV/3TC compared with the control treatments, given the observed effects of treatment on CD4 cell counts and HIV RNA levels, is 0.52, whereas the observed value was 0.16 (0.03-0.74). After adjustment for HIV RNA and CD4 changes over time the observed RH of progression to AIDS for ZDV/3TC treatment compared with controls was increased to 0.36 and was no longer significant (95% CI, 0.07-1.85).
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Enantiomerically pure carbocyclic 2'-deoxy-3'-azidothymidine monophosphate (AZTMP) and carba-2'deoxy-3'-thiocyanatothymidine monophosphate were synthesized to study their behavior toward their phosphorylation by thymidylate kinase. The nucleotides were synthesized starting from the parent nucleosides by an alkaline hydrolysis of the corresponding cycloSal-phosphate triesters.
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We propose that our models will accurately predict the extent of placental transfer of dideoxynucleoside drugs against human immunodeficiency virus. The models may also be applicable to other classes of drugs, regardless of therapeutic category, provided that these drugs passively diffuse across the placenta. Such a result will expedite phase 1 clinical trials of drugs in pregnant women.
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Certain antiretroviral medications for human immunodeficiency virus (HIV) have been implicated in increasing risk of cardiovascular disease. However, antiretroviral drugs are typically prescribed in combination. We characterized the association of current exposure to antiretroviral drug combinations on risk of cardiovascular events including myocardial infarction, stroke, percutaneous coronary intervention, and coronary artery bypass surgery. We used the Veterans Health Administration Clinical Case Registry to analyze data from 24 510 patients infected with HIV from January 1996 through December 2009. We assessed the association of current exposure to 15 antiretroviral drugs and 23 prespecified combinations of agents on the risk of cardiovascular event by using marginal structural models and Cox models extended to accommodate time-dependent variables.
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Recent findings suggest bidirectional antagonisms between the K65R mutation and thymidine analogue mutations in human immunodeficiency virus type 1 (HIV-1)-infected, treatment-experienced patients, yet little is known about HIV-2 in this regard. This study addressed the effects of innate polymorphisms in HIV-2 on emergent resistance to nucleoside/nucleotide analogues. Emergent drug resistance profiles in HIV-2 subtypes A (n = 3) and B (n = 1) were compared to those of HIV-1 subtypes B and C. Drug resistance was evaluated with cord blood mononuclear cells (CBMCs) and MT2 cells, using selective pressure with tenofovir (TFV), zidovudine (ZDV), stavudine (d4T), didanosine (ddI), abacavir (ABC), lamivudine (3TC), emtricitabine (FTC), or various dual-drug combinations. Resistance was evaluated using conventional and ultrasensitive sequencing approaches. In agreement with our previous findings, dual-drug combinations of TFV, ddI, ABC, d4T, ZDV, and 3TC preferentially selected for K65R in HIV-1 subtype C isolates. In HIV-1 subtype B, TFV-3TC and ZDV-3TC selected for M184I and D67N, respectively. In contrast, selections with all four HIV-2 cultures favored the development of M184I in dual-drug combinations that included either 3TC or FTC. Since HIV-2 cultures did not develop K65R, an ultrasensitive allele-specific real-time PCR assay was developed to distinguish the presence of 65R from wild-type K65 after 16 cycles with a discriminatory ability of 0.1% against a population of wild-type virus. These results underscore potential differences in emergent drug resistance pathways in HIV-1 and HIV-2 and show that polymorphisms may influence the development of the resistance pathways that are likely to emerge.
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Quantification and clinical evaluation of p24 antigen and anti-HIV antibody levels.
We identified an HIV-1 variant that belongs to the M group, with limited similarity of short genetic regions (100-200 nt) to subtype K, but the remainder of the genome is unrelated to any established HIV-1 subtype. The isolate was obtained from an HIV-1-positive male, living in the Netherlands, who encountered the virus before 1989, most probably via heterosexual contact in Africa. We describe the full-length genome sequence of four biological clones that were obtained from two samples collected 5 years apart. At both time points all open reading frames were intact. Within the 5-year interval, the person received antiretroviral therapy with zalcitabine and zidovudine for almost 4 years. Evolution of drug-resistant variants is likely given the increase in viral RNA load to +/-10,000 copies/ml during the last year of treatment. Surprisingly, the only regular RT mutation acquired during this period was K70R, which suggests that the genetic background of this variant is perhaps not suitable for the generation of the standard 41L, 67N, and 215Y/F mutations that typically arise during prolonged, nonsuccessful, zidovudine treatment. Awaiting the discovery of at least two additional, epidemiologically unrelated patients with a phylogenetically related HIV-1 variant, we can designate this variant a new HIV-1 subtype, or a distinct branch of subtype K.
A 49-year-old, human immunodeficiency virus-1-infected Asian woman developed Fanconi syndrome-like tubular acidosis while taking tenofovir disoproxil fumarate (TDF)/emtricitabine plus lopinavir/ritonavir for 9 months. All of her symptoms and abnormalities in laboratory tests resolved completely after switching TDF/emtricitabine to zidovudine and lamivudine. We consider that TDF caused symptomatic tubular acidosis in the present case, one of the few that has been reported in Japan to date.
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We studied the role of reverse transcriptase (RT) in human immunodeficiency virus (HIV)-1 replication in syncytia following cell fusion. A chronically HIV-1-infected MOLT-4 (MOLT-4/IIIB) cells allow HIV-1 replication and induce syncytium formation between uninfected MOLT-4 cells. AZT (3'-azido-3'-deoxythymidine, 1 microM) inhibited neither HIV-1 replication in MOLT-4/IIIB cells nor the syncytium formation induced by concultivation of MOLT-4/IIIB cells with uninfected MOLT-4 cells. In the supernatant of the syncytium containing culture a remarkably higher titer of p24 antigen was produced than in that of MOLT/IIIB cell culture. AZT inhibited p24 antigen production by HIV-1 in the syncytia to levels to comparable to that in MOLT-4/IIIB cells which were treated with AZT. In addition, p24 production by HIV-1 in the syncytia formed by cocultivation of CL-2 cells, which are chronically infected with HIV-1 but lack functional RT, with uninfected MOLT-4 cells was not different from that in CL-2 cells alone. The results suggest that HIV-1 RT plays an important role in HIV-1 replication within the syncytia but an RT-independent replication process which is essential for syncytium formation also exists in the syncytia. These results indicate that not only RT inhibitors but also inhibitors of syncytium formation are essential for anti-HIV therapy.
This review provides evidence that co-formulated abacavir-lamivudine-zidovudine remains a viable option for initiating antiretroviral therapy, especially in HIV-infected patients with pre-existing hyperlipidaemia. The varied geographical locations of the included trials augment the external validity of these findings. We are moderately confident in our estimate of the treatment effects of the triple NRTI regimen as initial therapy for HIV infection. In the context of the GRADE approach, such moderate quality of evidence implies that the true effects of the regimen are likely to be close to the estimate of effects found in this review; but there is a possibility that they could be substantially different. Further research should be geared towards defining the subgroup of HIV patients for whom this regimen will be most beneficial.