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  • HIV-1
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  • 1
    In: Journal of Clinical Microbiology, 2002, Vol. 40(4), p.1420
    Description: Combined antigen and antibody screening (fourth-generation) assays reduce the diagnostic window period between the time of human immunodeficiency virus (HIV) infection and laboratory diagnosis by 4 days, on average, in comparison to antibody-only (third generation) enzyme immunoassays (EIAs). The aim of the present study was to assess whether the new VIDAS HIV DUO Ultra (Biomerieux, Marcy-l'Etoile, France) showed an improved sensitivity and specificity in comparison to licensed fourth-generation assays. A total of 16 seroconversion panels, 15 cell culture supernatants infected with different HIV type 1 (HIV-1) subtypes, and 257 potentially cross-reactive serum samples were tested with VIDAS DUO HIV Ultra, Genscreen Plus HIV Ag-Ab, Enzygnost HIV Integral, Enzymun-Test HIV Combi, Genscreen HIV 1/2, version 2 (third-generation EIA), and Genetic Systems HIV-1 Ag EIA (p24 antigen assay). VIDAS HIV DUO Ultra showed a comparable sensitivity to the single p24 antigen assay in seroconversion panels and a dilution series of virus lysates. The diagnostic window was reduced with VIDAS HIV DUO Ultra by 3.82 days, on average, in comparison with the fourth- generation assay with the lowest sensitivity of the antigen detection module. HIV-1 infection was detected 5.88 days earlier than with third-generation EIA. The mean time delay between reverse transcription-PCR and VIDAS HIV DUO Ultra was only 2.31 days. The specificity of fourth-generation assays after retesting ranged between 98.1 and 100%. In conclusion, VIDAS HIV DUO Ultra can replace single-antigen screening for laboratory diagnosis and screening of HIV infection in blood donors. There was no evidence for a second diagnostic window due to impaired sensitivity of the antibody detection module of all the fourth- generation EIAs evaluated in the present study. The specificity after initial and/or repeated testing of VIDAS HIV DUO Ultra was equivalent to that of a third-generation assay.
    Keywords: Human Immunodeficiency Virus ; Human Immunodeficiency Virus ; Screening ; Immunoassays ; Antigens ; Antibodies ; Screening ; Immunoassays ; Antigens ; Antibodies ; AIDS: Immunological Aspects ; Viruses ; HIV ; HIV ; HIV;
    ISSN: 0095-1137
    ISSN: 00951137
    E-ISSN: 1098660X
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  • 2
    Language: English
    In: The Lancet, 1998, Vol.352(9122), pp.149-149
    Keywords: Medicine
    ISSN: 0140-6736
    E-ISSN: 1474-547X
    Source: ScienceDirect Journals (Elsevier)
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  • 3
    Language: English
    In: Medical Microbiology and Immunology, 2016, Vol.205(4), pp.315-320
    Description: Mutations in the genome of HIV-1 can compromise the success of antiretroviral treatments (ARTs) in HIV-1-infected individuals. The Frankfurt HIV Cohort Study Resistance Database (FHCS-RD) has previously documented a decline in the burden of resistance-associated mutations (RAMs) following the implementation of several new antiretroviral therapy regimens in 2007. In the current study, the annual burden of RAMs documented in the FHCS-RD in 2005–2013 was set in relation to the annual number of all cohort patients, drug regimens, available resistance tests, and prevalence for each RAM on relevant codons of reverse transcriptase (RT) and protease (PR) genes. A specific focus was put on the prevalence of the tenofovir disoproxil fumarate (TDF) signature mutation K65R in HIV-1 RT in relation to the application of TDF within ART. Between 2005 and 2012, a total of 4423 HIV genotyping data sets from 4509 patients were analysed. All mutations show a consistent decline, and the most impressive decrease was observed for thymidine analogue mutations (TAMs). The frequency of non-TAMs and PR mutations also decreased, but generally to a lower extent. The prevalence of K65R decreased from 2.6 % in 2005 to 0.2 % in 2012 despite increased use of TDF-containing ART. Both the improved strategic use of TDF in ARTs and generally more effective ART regimens may have resulted in decreasing RAM prevalences in FHCS-RD since 2007. These trends challenge the cost-effectiveness of resistance testing prior to failing ART.
    Keywords: Frankfurt HIV Cohort Study ; Tenofovir disoproxil fumarate ; RAM ; Prevalence ; K65R
    ISSN: 0300-8584
    E-ISSN: 1432-1831
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  • 4
    Language: English
    In: HIV Clinical Trials, 01 August 2013, Vol.14(4), pp.175-184
    Description: Background: Immune response rates following influenza vaccination are often lower in HIV-infected individuals. Low vitamin D levels were correlated with weak immune response in cancer patients and are known to be lower in HIV-infected patients....
    Keywords: Adjuvanted ; Hemagglutination Inhibition Assay ; HIV ; H1n1 ; Memory Response ; Trivalent Influenza Vaccine ; Vitamin D ; Medicine
    ISSN: 1528-4336
    E-ISSN: 1945-5771
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  • 5
    Language: English
    In: Scandinavian Journal of Infectious Diseases, 01 September 2014, Vol.46(9), pp.656-659
    Description: The immune response after influenza vaccination is impaired in HIV-infected individuals and can be enhanced by a second dose. The durability of the antibody protection and its clinical benefit is not known. We investigated clinical symptoms...
    Keywords: HIV ; H1n1 ; Adjuvanted ; Pandemic ; Durability ; Medicine
    ISSN: 0036-5548
    E-ISSN: 1651-1980
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  • 6
    In: Antimicrobial Agents and Chemotherapy, 2003, Vol. 47(1), p.54
    Description: Zidovudine resistance (ZDV-R) is associated with classic genotypic changes at codons 41, 67, 70, 210, 215, and 219 of the human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT) gene as well as with the multinucleoside resistance (MNR) complexes (Q151M MNR complex; 6-bp insertion/A62V complex). In addition, enhanced resistance to ZDV in the context of the classic ZDV mutations plus the M184V mutation has been associated with additional mutations at positions 208, 211, 214, and 333. In this study we investigated phenotypic ZDV-R determined by a recombinant virus assay (Antivirogram; Virco) in 223 clinical samples in relation to the above genotypic changes. 150 out of 223 clinical samples had the M184V mutation. Phenotypic ZDV-R ranged from 0.3- to 5,338-fold. Sixteen samples (15 with high ZDV-R ranging from 90- to 3,571-fold) contained MNR-associated patterns. Analysis of classic mutational patterns broadly demonstrated increasing ZDV-R with increasing number of ZDV mutations. A comparable correlation was obtained when ZDV-R was analyzed only relative to the T215Y/F mutation. Site-directed mutagenesis experiments investigating the influence of the additional mutations H208Y, R211K, and L214F on ZDV-R resulted in a 7.4- or 21-fold increase in ZDV-R when the R211K/L214F or H208Y/R211K/L214F mutations, respectively, were added to a highly ZDV-R virus. In the clinical sample data set we analyzed, the combination of R211K/L214F appeared most frequently. The H208Y change was detected only in highly ZDV-R viruses, whereas the G333E/D change was distributed equally. All changes were independent of the M184V mutation. A 2.4- or 8-fold increase in ZDV-R was observed in the clinical samples with high ZDV-R containing the R211K/L214F or H208Y/R211K/L214F mutations, respectively. We have shown that the combination of the additional mutations H208Y, R211K, and L214F in HIV-1 RT may influence ZDV-R and should be considered when assessing ZDV-R.
    Keywords: Drug Resistance, Viral -- Genetics ; HIV-1 -- Genetics ; RNA-Directed DNA Polymerase -- Genetics ; Zidovudine -- Pharmacology;
    ISSN: 0066-4804
    ISSN: 00664804
    E-ISSN: 10986596
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  • 7
    Language: English
    In: Expert Review of Molecular Diagnostics, 01 May 2007, Vol.7(3), pp.237-246
    Description: Infection with HIV results in lifelong persistence of the virus in the body of infected persons, independent of antiretroviral treatment. Therefore, efficient and meaningful therapy monitoring has been developed since its introduction in the 1980s. Whereas, primarily, the measurement of the CD4 cell count was the most important clinical marker of disease progression, nowadays the estimation of plasma viral load with molecular methods plays a major role as a marker of therapy success. To optimize therapy changes in patients failing on antiretroviral therapy regimen, HIV-1 genotyping has been introduced and is now widely accepted as an additional diagnostic tool. Due to this increase in diagnostic parameters, clinicians and virologists have to cope with many different methods. This review should give a brief overview of the current commercially available assays for detection and quantification of HIV, as well as for HIV-1 genotypic resistance testing. Quantitative reverse transcriptase PCR, real-time PCR, nucleic acid sequence-based amplification and the branched DNA system are described in detail, and the advantages and disadvantages are discussed. In addition, two commercially available HIV-1 genotyping assays are compared. However, a general recommendation to favor one system over the other cannot be given, because the final decision of which system to use should be decided on the individual requirements.
    Keywords: Bdna ; HIV-1 Genotyping ; HIV-1 Monitoring ; Nasba ; Real-Time Pcr ; Rt-Pcr ; Viral Load ; Medicine
    ISSN: 1473-7159
    E-ISSN: 1744-8352
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  • 8
    Language: English
    In: Clinical chemistry, July 2006, Vol.52(7), pp.1258-66
    Description: Current HIV-1 viral-load assays are too expensive for resource-limited settings. In some countries, monitoring of antiretroviral therapy is now more expensive than treatment itself. In addition, some commercial assays have shown shortcomings in quantifying rare genotypes. We evaluated real-time reverse transcription-PCR with internal control targeting the conserved long terminal repeat (LTR) domain of HIV-1 on reference panels and patient samples from Brazil (n = 1186), South Africa (n = 130), India (n = 44), and Germany (n = 127). The detection limit was 31.9 IU of HIV-1 RNA/mL of plasma (〉 95% probability of detection, Probit analysis). The internal control showed inhibition in 3.7% of samples (95% confidence interval, 2.32%-5.9%; n = 454; 40 different runs). Comparative qualitative testing yielded the following: Roche Amplicor vs LTR assay (n = 431 samples), 51.7% vs 65% positives; Amplicor Ultrasensitive vs LTR (n = 133), 81.2% vs 82.7%; BioMerieux NucliSens HIV-1 QT (n = 453), 60.5% vs 65.1%; Bayer Versant 3.0 (n = 433), 57.7% vs 55.4%; total (n = 1450), 59.0% vs 63.8% positives. Intra-/interassay variability at medium and near-negative concentrations was 18%-51%. The quantification range was 50-10,000,000 IU/mL. Viral loads for subtypes A-D, F-J, AE, and AG yielded mean differences of 0.31 log(10) compared with Amplicor in the 10(3)-10(4) IU/mL range. HIV-1 N and O were not detected by Amplicor, but yielded up to 180 180.00 IU/mL in the LTR assay. Viral loads in stored samples from all countries, compared with Amplicor, NucliSens, or Versant, yielded regression line slopes (SD) of 0.9 (0.13) (P 〈 0.001 for all). This method offers all features of commercial assays and covers all relevant genotypes. It could allow general monitoring of antiretroviral therapy in resource-limited settings.
    Keywords: HIV Long Terminal Repeat ; HIV-1 ; Viral Load ; Reverse Transcriptase Polymerase Chain Reaction -- Methods
    ISSN: 0009-9147
    E-ISSN: 15308561
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  • 9
    Language: English
    In: FEBS Letters, 2002, Vol.516(1), pp.43-46
    Description: DOCK and Affinity studies were carried out to study the binding of D - and L -penicillamine to the transactivator protein (tat) of human immunodeficiency virus type 1 (HIV-1). These studies reveal a selective binding of D -penicillamine to the cysteine-rich region covering amino acid residues 20–38 of the tat protein. A careful analysis of the components of the binding energy of the D - and L -isomers reveals that the D -isomer has a more favorable van der Waals interaction resulting from an optimal placement of the dimethylthiomethyl side chain in the binding site. This observation matches the experimental data that D -penicillamine is a more potent inhibitor of tat-mediated transactivation than the L -isomer. The docking and experimental data offer an interesting approach to design structural molecules with potential application to block signal functions of the tat protein in HIV-1 pathogenesis.
    Keywords: D-Penicillamine ; Human Immunodeficiency Virus Type 1 Transactivation ; Tat Protein ; Docking ; Biology ; Chemistry ; Anatomy & Physiology
    ISSN: 0014-5793
    E-ISSN: 1873-3468
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  • 10
    Language: English
    In: Antimicrobial agents and chemotherapy, September 2007, Vol.51(9), pp.3264-72
    Description: The objective of this study was to identify parameters among saquinavir pharmacokinetics, patients' demographics or comedications, to be addressed for improved personalized therapy. The presence of human immunodeficiency virus type 1 (HIV-1) RNA at therapy week 48 (principal target parameter), CD4 cell count at week 48, infections and side effects during 48 weeks, indicators of liver toxicity and lipid abnormalities at week 48, and a 12-h saquinavir plasma concentration-versus-time profile were assessed in 56 patients receiving saquinavir-ritonavir (1,000 and 100 mg, respectively) twice daily (44 therapy-naïve and 12 antiretrovirally pretreated patients) for association with saquinavir plasma concentrations, demographics, baseline values of target parameters, and coadministered antiretrovirals. Antiretroviral failure was observed in 8 of the 56 patients in whom HIV-1 RNA was detectable at week 48. This therapeutic failure was not associated with individual saquinavir pharmacokinetics. More likely, therapeutic failure was related to incidences interfering with antiretroviral therapy, causing therapy interruptions or incompliance. Weak associations were, however, seen between high maximum saquinavir plasma concentrations and both CD4 counts of 〉 or =200 cells microl(-1) at week 48 (P = 0.014) and constitutional side effects during 48 weeks (P = 0.002). However, patients with high CD4 counts and constitutional side effects were not identical (P = 0.53). Saquinavir therapeutic drug monitoring in patients infected with protease inhibitor-susceptible HIV-1 taking saquinavir-ritonavir (1,000 and 100 mg, respectively) is not demanded for improving the antiretroviral effect. It may be contemplated in cases with constitutional side effects or low CD4 counts with weak immune responses.
    Keywords: HIV Infections -- Drug Therapy ; HIV Protease Inhibitors -- Adverse Effects ; HIV-1 -- Drug Effects ; Saquinavir -- Adverse Effects
    ISSN: 0066-4804
    Source: MEDLINE/PubMed (U.S. National Library of Medicine)
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