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  • Efavirenz-Based Antiretroviral Therapy Among Nevirapine-Exposed HIV-Infected Children in South Africa: A Randomized Clinical Trial

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    JAMA. 2015; 314(17):1808-1817. doi: 10.1001/jama.2015.13631

    This randomized trial compares risks of viral rebound and viral failure with continuation of ritonavir-boosted lopinavir vs switching to efavirenz among children with human immunodeficiency virus (HIV) infection exposed to nevirapine for prevention of mother-to-child transmission who had initial viral suppression with ritonavir-boosted lopinavir–based therapy.

  • Antiretroviral Therapy for Nevirapine-Exposed Children With HIV Infection

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    JAMA. 2015; 314(17):1801-1802. doi: 10.1001/jama.2015.13763
  • Association Between Efavirenz-Based Compared With Nevirapine-Based Antiretroviral Regimens and Virological Failure in HIV-Infected Children

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    JAMA. 2013; 309(17):1803-1809. doi: 10.1001/jama.2013.3710
    Lowenthal and coauthors report on the association between efavirenz-based vs nevirapine-based antiretroviral regimens and virological failure in children infected with human immunodeficiency virus.
  • Reuse of Nevirapine in Exposed HIV-Infected Children After Protease Inhibitor–Based Viral Suppression: A Randomized Controlled Trial

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    JAMA. 2010; 304(10):1082-1090. doi: 10.1001/jama.2010.1278
  • Coverage of Nevirapine-Based Services to Prevent Mother-to-Child HIV Transmission in 4 African Countries

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    JAMA. 2010; 304(3):293-302. doi: 10.1001/jama.2010.990
  • JAMA July 21, 2010

    Figure 2: Cascade of Events Negotiated by Mothers Infected With Human Immunodeficiency Virus (HIV) and Their HIV-Exposed Infants to Prevent Mother-to-Child HIV Transmission

    This figure demonstrates the critical path (or cascade) that members of the surveillance population negotiated to prevent (or fail to prevent) mother-to-child HIV transmission. Step A (upper bar) represents all the women in the surveillance population who were seropositive at delivery. Steps C through G represent a critical path, each of which is contingent on the previous one being successfully negotiated. Coverage, defined as the proportion of infected or exposed mother-infant pairs who received both the maternal and infant nevirapine doses, was 1725/3196 or 54% (this estimate is not weighted for country [see “Methods” section]). There were 240 cases for whom we know coverage failed (because there was no nevirapine in the cord blood) but due to inadequate documentation in the antenatal record, we could not ascertain the reason for the failure. Step H is not contingent on steps E, F, or G; an additional 621 HIV-exposed infants were administered nevirapine prior to discharge who had cord blood that was not positive for nevirapine at delivery. Thus, these infants were not included in the primary outcome measure.
  • Outcomes of Nevirapine- and Efavirenz-Based Antiretroviral Therapy When Coadministered With Rifampicin-Based Antitubercular Therapy

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    JAMA. 2008; 300(5):530-539. doi: 10.1001/jama.300.5.530
  • JAMA August 16, 2006

    Figure 3: Cumulative Rate (Proportion) of Infant End Points (Original Study Period)

    Cumulative event rate during the original study period (births prior to August 12, 2002), where for each end point a significant interaction between the 2 randomized factors (perinatal intervention of active nevirapine to mothers/infants [mother-nevirapine/infant-nevirapine] vs placebo [mother-placebo/infant-placebo] and feeding strategy) was detected; analyses include 121 infants assigned to formula feeding and placebo/placebo, 121 infants assigned to breastfeeding plus zidovudine and placebo/placebo, 124 infants assigned to formula feeding and nevirapine/nevirapine, and 119 infants assigned to breastfeeding plus zidovudine and nevirapine/nevirapine. Rates over time are calculated from the Kaplan-Meier method. P values are based on stratified log rank test (efficacy end points), log rank test (mortality), and the Cox model (interaction).
  • JAMA August 16, 2006

    Figure 2: Cumulative Rate (Proportion) of Infant End Points (Entire Study and Revised Study Period)

    HIV denotes human immunodeficiency virus. Top row (panels A,B,C) shows cumulative event rate by randomized feeding strategy (and collapsing over peripartum groups) over the entire study period (including 591 infants assigned to the formula-fed group and 588 infants assigned to the breastfed plus zidovudine group). Bottom row (panels D, E, F) shows cumulative event rate for the revised study period (births after August 12, 2002) reflecting change in perinatal intervention study group (active, open-label nevirapine to all infants and availability of HAART to qualifying mothers and infants). The analyses in the bottom row consist of 348 infants assigned to the breastfed plus zidovudine group including 177 whose mothers were assigned to single-dose placebo, and 346 infants assigned to the formula-fed group including 172 whose mothers were assigned to single-dose placebo. Rates over time are calculated from the Kaplan-Meier method. P values are based on stratified log rank test (efficacy end points) and log rank test (mortality).
  • Reducing HIV Vertical Transmission Scrutinized

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    JAMA. 2005; 293(17):2079-2081. doi: 10.1001/jama.293.17.2079
  • JAMA February 16, 2005

    Figure 1: Blips and Drug Levels

    Plasma human immunodeficiency virus 1 (HIV-1) RNA levels, plasma concentrations of protease and nonnucleoside reverse transcriptase inhibitors, and suggested minimum target trough concentration (as provided by drug manufacturers), for each of the 10 patients. Data markers below the black dotted line indicate undetectable levels of plasma HIV-1 RNA (<50 copies/mL). Patients were sampled 36 times. For each sample, viral RNA was measured in 2 independent laboratories. For each time point, the higher value was plotted. A total of 720 viral load measurements were expected (36 time points × 2 independent measurements × 10 patients). Of these, 713 were collected (99.03%). Of planned assays for plasma drug concentration, 98.33% were completed. M8 is the measurable active metabolite of nelfinavir. EFV indicates efavirenz; LPV, lopinavir; NFV, nelfinavir; NVP, nevirapine; RTV, ritonavir; SQV, saquinavir.
  • JAMA February 16, 2005

    Figure 2: Lack of New Genotypic Resistance Mutations in Plasma Virus During or Immediately After Blips

    At all points other than those at which the plasma HIV-1 RNA level was ≥50 copies/mL, the viral load was undetectable. Up to 7 independent clones were obtained at each time point. Note that no new mutations conferring drug resistance appeared during the blips. All mutations detected during or within 30 days after blips were present at baseline (B) or were seen in plasma samples taken prior to the blips. Baseline mutations were identified in either plasma or resting CD4 cell reservoir samples (peripheral blood). The resting cell reservoir was sampled only at baseline. “Prior ART exposure” refers to other antiretroviral drugs the patient has taken that are not part of the current regimen. ABC indicates abacavir; ADF, adefovir; APV, amprenavir; ART, antiretroviral therapy; AZT, zidovudine; ddC, zalcitabine; ddI, didanosine; d4T, stavudine; EFV, efavirenz; HAART, highly active antiretroviral therapy; HIV, human immunodeficiency virus; IDV, indinavir; LPV, lopinavir; NFV, nelfinavir; NNRTI, nonnucleoside reverse transcriptase inhibitor; NRTI, nucleoside reverse transcriptase inhibitor; NVP, nevirapine; PI, protease inhibitor; RTV, ritonavir; SQV, saquinavir; TDF, tenofovir disoproxil fumarate; 3TC, lamivudine; WT, wild type.
  • Nevirapine and Zidovudine at Birth to Reduce Perinatal Transmission of HIV in an African Setting: A Randomized Controlled Trial

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    JAMA. 2004; 292(2):202-209. doi: 10.1001/jama.292.2.202
  • JAMA July 14, 2004

    Figure: Study Flow of Participating Women and Infants

    HIV indicates human immunodeficiency virus; NVP, nevirapine; ZDV, zidovudine; ELISA, enzyme-linked immunosorbent assay.*These women declined to speak with the counselor regarding counseling about HIV and the study.
  • Treatment for Adult HIV Infection: 2004 Recommendations of the International AIDS Society-USA Panel

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    JAMA. 2004; 292(2):251-265. doi: 10.1001/jama.292.2.251
  • Two-Dose Intrapartum/Newborn Nevirapine and Standard Antiretroviral Therapy to Reduce Perinatal HIV Transmission: A Randomized Trial

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    JAMA. 2002; 288(2):189-198. doi: 10.1001/jama.288.2.189
  • Serious Adverse Events Attributed to Nevirapine Regimens for Postexposure Prophylaxis After HIV Exposures—Worldwide, 1997-2000

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    JAMA. 2001; 285(4):402-403. doi: 10.1001/jama.285.4.402
  • JAMA May 10, 2000

    Figure: Most Common Mutations in HIV-1 Genes Conferring Drug Resistance

    For each amino acid residue, the letter above indicates the amino acid associated with wild-type virus; the italicized letters below, substitutions that confer viral resistance. Primary mutations (black bars) generally cause decreased inhibitor binding and are the first mutations selected. Secondary mutations (white bars) also contribute to drug resistance and should be considered as evidence of resistance, although they may have less direct effect on inhibitor binding in vitro than primary mutations. The mutation selected in vitro (black-and-white bar) is rarely seen in patients having treatment failure. For indinavir, the mutations listed as primary may not be the first mutations selected, but they are selected in most patient isolates in combination with other mutations. For zalcitabine, all mutations are listed as primary because of inadequate clinical data to determine the most frequent initial mutation. Amino acid abbreviations are: A, alanine; C, cysteine; D, aspartate; E, glutamate; F, phenylalanine; G, glycine; H, histidine; I, isoleucine; K, lysine; L, leucine; M, methionine; N, asparagine; P, proline; Q, glutamine; R, arginine; S, serine; T, threonine; V, valine; W, tryptophan; Y, tyrosine. Multinucleoside resistance mutational patterns A and B each cause resistance to zidovudine, stavudine, lamivudine, didanosine, zalcitabine, and abacavir. Current listings are also available at http://www.iasusa.org/.*Mutations selected by protease inhibitors in gag cleavage sites are not listed because their contribution to resistance is not fully defined.† A preliminary report identifies mutations E44D and V118I as conferring moderately reduced (about 10-fold) susceptibility to lamivudine with uncertain clinical significance. This contrasts with the greater than 100-fold reduced susceptibility to lamivudine conferred by M184V or M184I, which is associated with virologic rebound.‡ The mutations listed for zidovudine above contribute to reduced susceptibility to abacavir in vitro and in vivo and are listed as secondary, even though they may be present before abacavir is introduced. They have also been reported to be uncommonly selected by stavudine plus didanosine even in the absence of prior zidovudine exposure. Phenotypic resistance of these mutations to stavudine or didanosine in vitro was not identified. The clinical significance of these mutations and of V75T on in vivo response to stavudine is not known.§ Several insertions of 2 amino acids have been reported following T69S (or rarely T69A), including Ser-Ser; Ser-Gly; Ser-Ala; Glu-Ala; and Thr-Ser.∥ For nevirapine or delavirdine, each mutation can occur as an initial or subsequent mutation and affect inhibitor binding.
  • JAMA September 22, 1999

    Figure 1: Human Immunodeficiency Virus 1 Samples With Reduced Susceptibility to Antiretroviral Drugs

    The percentages of patient viral samples that exhibited a greater than 10-fold (black) or greater than 2.5- to 10-fold (gray) level of reduced susceptibility at baseline to nucleoside reverse transcriptase inhibitors (NRTIs), nonnucleoside reverse transcriptase inhibitors (NNRTIs), and protease inhibitors (PIs) are shown. Asterisks indicate a significant difference between the measured frequencies of reduced susceptibilities for nevirapine and efavirenz (P<.001), delavirdine and efavirenz (P<.001), nelfinavir and saquinavir (P=.002), and nelfinavir and indinavir (P=.002).
  • JAMA June 24, 1998

    Figure: Antiretroviral Drug Resistance Testing in Adults With HIV Infection: Implications for Clinical Management

    Figure 1.—The most common human immunodeficiency virus 1 mutations selected by protease inhibitors (A), and nucleoside and nonnucleoside reverse transcriptase inhibitors (B). For each amino acid residue listed, the letter above the listing indicates the amino acid associated with the wild-type virus. The italicized letter below the residue indicates the substitution that confers drug resistance. The drug-selected mutations are categorized as "primary" (black bars) or "secondary" (white bars). (The black-and-white bar indicates a mutation selected in vitro, but rarely seen in specimens from patients in whom therapy fails.) Primary mutations generally decrease inhibitor binding and are the first mutations selected. For indinavir, the mutations listed as primary may not be the first mutations selected, but they are selected in most patients' isolates in combination with other mutations. For zalcitabine, all mutations are listed as secondary because of inadequate clinical data to determine a common initial mutation. For nevirapine and delavirdine, each mutation can occur as either an initial or subsequent mutation and affect inhibitor binding. The asterisk indicates that the mutation has been reported in vitro, but relevance for clinical drug failure is uncertain. Amino acid abbreviations are as follows: A, alanine; C, cysteine; D, aspartate; E, glutamate; F, phenylalanine; G, glycine; H, histidine; I, isoleucine; K, lysine; L, leucine; M, methionine; N, asparagine; P, proline; Q, glutamine; R, arginine; S, serine; T, threonine; V, valine; W, tryptophan; Y, tyrosine. Multinucleoside resistance viruses have phenotypic resistance to most nucleoside reverse transcriptase inhibitors. Current listings are also available at http://hiv-web.lanl.gov/ or at http://www.viral-resistance.com.