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  • JAMA August 16, 2006

    Figure 1: Time Line for the Course of HIV Disease and Metabolic and Skeletal Complications for the Patient in the Case Presentation

    Dates in this time line are approximate. Table shows selected laboratory data; blank cells indicate no data. Selected medications, including antiretroviral drugs, and clinical events are indicated graphically. Lengths of bars are scaled according to dates of laboratory measurements and do not accurately reflect duration. ABC indicates abacavir; D4T, stavudine; DDI, didanosine; HIV, human immunodeficiency virus; IDV, indinavir; LPV, lopinavir; NFV, nelfinavir; NRTI, nucleoside reverse transcriptase inhibitor; RTV, ritonavir; TDF, tenofovir; and 3TC, lamivudine.
  • 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.
  • Dual vs Single Protease Inhibitor Therapy Following Antiretroviral Treatment Failure: A Randomized Trial

    Abstract Full Text
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    JAMA. 2002; 288(2):169-180. doi: 10.1001/jama.288.2.169
  • JAMA July 10, 2002

    Figure 2: Viral Load and CD4 Cell Count Change From Baseline in Dual Protease Inhibitor and Placebo Arms

    Dual protease inhibitor arms received saquinavir, indinavir, and nelfinavir. All patients also received amprenavir, abacavir, efavirenz, and adefovir dipivoxil.
  • JAMA October 3, 2001

    Figure: Proportion of Overlapping Cisapride and Contraindicated Drug Pairs (N = 4414)

    Drugs are only counted as contraindicated beginning with the month in which the prescription label first states they are contraindicated. Records were not included if prescriber data or pharmacy data were missing for either the cisapride prescription or the contraindicated prescription. Physician notification letters listing coprescription warnings were issued for February 1995 (azole antifungals [fluconazole, ketoconazole, itraconazole]), October 1995 (macrolide antibiotics [clarithromycin, erythromycin, troleandomycin, miconazole IV]), and June 1998 (protease inhibitors [indinavir, ritonavir] and antidepressants [nefadozone]). The instability in early 1995 reflects the small number of prescriptions for azole antifungals, which were the only contraindicated drugs until October 1995.
  • JAMA July 11, 2001

    Figure 2: HIV-1 Reverse Transcriptase Sequences Amplified From Plasma

    HAART indicates highly active antiretroviral therapy; HIV-1, human immunodeficiency virus type 1; AZT, zidovudine; ddI, didanosine; 3TC, lamivudine; d4T, stavudine; ABC, abacavir; DLV, delavirdine; EFV, efavirenz; RTV, ritonavir; NFV, nelfinavir; SQV, saquinavir; and IDV, indinavir. For protease drug resistance color codes, see Figure 3. Accessory mutation refers to a genetic variant that alone does not confer high-level resistance but can occur in association with resistance mutations and may contribute to resistance or viral fitness. *Indicates insertion sequences.
  • Abacavir-Lamivudine-Zidovudine vs Indinavir-Lamivudine-Zidovudine in Antiretroviral-Naive HIV-Infected Adults: A Randomized Equivalence Trial

    Abstract Full Text
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    JAMA. 2001; 285(9):1155-1163. doi: 10.1001/jama.285.9.1155
  • JAMA March 7, 2001

    Figure 2: Plasma Human Immunodeficiency Virus (HIV) RNA Levels

    Asterisk indicates intent-to-treat analysis. Two patients in the abacavir group and 2 patients in the indinavir group had missing plasma samples (panels A and C).
  • JAMA March 7, 2001

    Figure 1: Profile of Patient Enrollment and Discontinuations Through 48 Weeks of Treatment

    Patients who did not receive intervention failed to return to the clinic prior to the first dose. Other reasons for study discontinuation included protocol violations, clinical progression, deaths, and unspecified reasons. Three deaths occurred in the abacavir group; 1 was due to hypersensitivity reaction following rechallenge with abacavir and 2 for reasons unrelated to study drugs. One death occurred in the indinavir group for reasons unrelated to study drugs.
  • 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*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 January 12, 2000

    Figure: Indinavir Susceptibility During Viral Rebound of Subject 12 While Receiving Triple-Drug Therapy of Indinavir, Zidovudine, and Lamivudine

    The baseline and 4 isolates tested during rebound at weeks 30, 36, 46, and 61 remained sensitive (S) to indinavir. Indinavir levels were detectable at all time points tested except week 8, which immediately preceded loss of viral suppression.
  • Mechanisms of Virologic Failure in Previously Untreated HIV-Infected Patients From a Trial of Induction-Maintenance Therapy

    Abstract Full Text
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    JAMA. 2000; 283(2):205-211. doi: 10.1001/jama.283.2.205
  • Drug Susceptibility in HIV Infection After Viral Rebound in Patients Receiving Indinavir-Containing Regimens

    Abstract Full Text
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    JAMA. 2000; 283(2):229-234. doi: 10.1001/jama.283.2.229
  • JAMA January 12, 2000

    Figure 1: Ratio of Plasma Indinavir Levels to Expected Levels in First Plasma Sample (S1) and Second Plasma Sample (S2)

    Lines between circles or triangles correspond to the same patient. In the triple-drug group (zidovudine, lamivudine, and indinavir), cases had indinavir concentration ratios significantly lower than those of controls (S1, P = .02; S2, P<.01). In the zidovudine-indinavir group, no statistical difference between cases and controls was seen at S1 (P = .35) but was observed at S2 (P = .04). The S1 sample corresponds to initial virologic failure. The S2 sample was obtained 6 weeks after S1 for confirmation of viral rebound. The gray line indicates an indinavir ratio of 0.6, which corresponds to the lowest value of expected indinavir level, taking into account intersubject variability (see "Adherence Assessment" section). Samples for S1 and S2 were not paired for some cases and controls.
  • JAMA January 12, 2000

    Figure 2: Viral Load Rebound of First Plasma Sample (S1) and Second Plasma Sample (S2)

    Viral load rebound defined as plasma human immunodeficiency virus (HIV) RNA level in the S1 or S2 specimen after subtraction of the baseline level by treatment group (the zidovudine-indinavir group is split according to the plasma indinavir ratio) and by S1 or S2. Indinavir-0 patients have at least 1 indinavir ratio below 0.6; indinavir-1 patients have individual level within normal range. The line at 0 indicates that viral rebound is exactly equal to the baseline value. Horizontal bar indicates median; box, interquartile range; and error bars, 95% confidence interval.
  • Resistance, Fitness, Adherence, and Potency: Mapping the Paths to Virologic Failure

    Abstract Full Text
    JAMA. 2000; 283(2):250-251. doi: 10.1001/jama.283.2.250
  • JAMA January 5, 2000

    Figure 1: Incidence Rate (Cases per Persons Exposed) of Hepatotoxicity During Antiretroviral Therapy, by Drug Regimen

    Antiretroviral treatment categories are ritonavir-containing regimens, including ritonavir and ritonavir plus saquinavir; nonritonavir protease inhibitor regimens, including indinavir, nelfinavir, and saquinavir; and dual nucleoside analog (nonprotease inhibitor) regimens. Hepatotoxicity is categorized using a standardized toxicity grade scale.
  • JAMA September 22, 1999

    Figure 3: Longitudinal Determinations of Plasma HIV RNA, Plasma-Derived HIV-1 Genotypes, and Selected Phenotypes of Plasma-Derived Recombinant Viruses

    Data are from subject multidrug-resistant 1 with resistance to lamivudine at baseline who was treated with zidovudine-lamivudine-indinavir. Resistance of recombinant viruses to indinavir (circle), nelfinavir (square), and ritonavir (diamond) at days 0, 260, 400, and 730 of therapy are shown. HIV-1 indicates human immunodeficiency virus 1; RT, reverse transcriptase; PR, protease; and WT, wild type.
  • 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 September 22, 1999

    Figure 3: Response to Therapy for 1 Patient With A Drug-Resistant Human Immunodeficiency Virus (HIV) Strain Compared With a Patient With Wild-type HIV

    The virological response to therapy for patient 98-1186 (red triangle), with a greater than 10-fold reduction in drug susceptibility, is compared with a typical patient (97-513, blue diamond) with wild-type drug susceptibility. Both subjects initiated combination antiretroviral therapy with zidovudine-lamivudine-indinavir within 7 days of study entry. Genotypic sequence analysis for patient 98-1186 was performed on a sample collected 49 days after the start of therapy (study day 53). Well-recognized drug resistance mutations for zidovudine, lamivudine, and multiple protease inhibitors were identified. Antiretroviral therapy was changed on study day 89 to didanosine-stavudine-efavirenz-abacavir, with hydroxyurea added 54 days later (day 143). Complete suppression of viral load (HIV RNA <50 copies/mL) was first documented approximately 11 weeks after changing antiretroviral therapy. Gray line indicates lower limit of detection of viral load.