Publications
321 results found
Mackie NE, Fidler S, Tamm N, et al., 2004, Clinical implications of stopping nevirapine-based antiretroviral therapy: relative pharmacokinetics and avoidance of drug resistance, HIV MEDICINE, Vol: 5, Pages: 180-184, ISSN: 1464-2662
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- Citations: 48
Balla-Jhagjhoorsingh SS, Koopman G, Mooij P, et al., 2004, Long-term persistence of HIV-1 vaccine-induced CD4<SUP>+</SUP>CD45RA<SUP>-</SUP>CD62L<SUP>-</SUP>CCR7<SUP>-</SUP> memory T-helper cells, AIDS, Vol: 18, Pages: 837-848, ISSN: 0269-9370
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- Citations: 6
White NC, Israel-Biet D, Coker RJ, et al., 2004, Different resistance mutations can be detected simultaneously in the blood and the lung of HIV-1 infected individuals on antiretroviral therapy, JOURNAL OF MEDICAL VIROLOGY, Vol: 72, Pages: 352-357, ISSN: 0146-6615
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- Citations: 8
Goon PKC, Igakura T, Hanon E, et al., 2004, Human T cell lymphotropic virus type I (HTLV-I)-specific CD4<SUP>+</SUP> T cells:: Immunodominance hierarchy and preferential infection with HTLV-I, JOURNAL OF IMMUNOLOGY, Vol: 172, Pages: 1735-1743, ISSN: 0022-1767
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- Citations: 58
Sukhanova AL, Kazennova EV, Rudinskiĭ NI, et al., 2004, [The genetic variability of the protease-encoding region in HIV-1 A isolates and in CRF03_AB recombinants as observed in the CIS territory]., Vopr Virusol, Vol: 49, Pages: 4-9, ISSN: 0507-4088
Protease-encoding nucleotide sequences of 27 HIV-1 variants isolated in Russia and other CIS countries from seropositive intravenous drug-users were analyzed. None of the above persons did ever take antiretroviral drugs. The nucleotide sequences were shown to belong to subtypes A and to be have a high degree of genetic homogeneity (0.00-3.23; mean--1.38 +/- 0.79). No isolates contained any primary mutations of resistance to protease inhibitors. At the same time, above one half of the isolates bore the V771 substitution, which, according to published data, is the secondary mutation of resistance that conditions a higher resistance to Nelfinavir. Moreover, the substitution was associated with 2 synonymous mutations in triplets 31 and 78, which denotes a single origin for all V771 variants.
Ward H, Weber J, 2003, Validity and utility of screening tests for STIs, SEXUALLY TRANSMITTED INFECTIONS, Vol: 79, Pages: 356-357, ISSN: 1368-4973
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- Citations: 1
Piñon JD, Klasse PJ, Jassal SR, et al., 2003, Human T-cell leukemia virus type 1 envelope glycoprotein gp46 interacts with cell surface heparan sulfate proteoglycans, JOURNAL OF VIROLOGY, Vol: 77, Pages: 9922-9930, ISSN: 0022-538X
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- Citations: 82
Goon PKC, Igakura T, Hanon E, et al., 2003, High circulating frequencies of tumor necrosis factor alpha- and interleukin-2-secreting human T-lymphotropic virus type 1 (HTLV-1)-specific CD4<SUP>+</SUP> T cells in patients with HTLV-1-associated neurological disease, JOURNAL OF VIROLOGY, Vol: 77, Pages: 9716-9722, ISSN: 0022-538X
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- Citations: 48
Hodgson TA, Fidler SJ, Speight PM, et al., 2003, Oral pemphigus vulgaris associated with HIV infection, JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY, Vol: 49, Pages: 313-315, ISSN: 0190-9622
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- Citations: 9
Saito M, Braud VM, Goon P, et al., 2003, Low frequency of CD94/NKG2A<SUP>+</SUP> T lymphocytes in patients with HTLV-1-associated myelopathy/tropical spastic paraparesis, but not in asymptomatic carriers, BLOOD, Vol: 102, Pages: 577-584, ISSN: 0006-4971
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- Citations: 22
Beddows S, Galpin S, Kazmi SH, et al., 2003, Performance of two commercially available sequence-based HIV-1 genotyping systems for the detection of drug resistance against HIV type 1 group M subtypes, JOURNAL OF MEDICAL VIROLOGY, Vol: 70, Pages: 337-342, ISSN: 0146-6615
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- Citations: 37
Snoeck J, Kantor R, Shafer RW, et al., 2003, Comparison of five interpretation algorithms for the prediction of protease inhibitor susceptibility in HIV-1 non-B subtypes, 12th International HIV Drug Resistance Workshop, Publisher: INT MEDICAL PRESS LTD, Pages: U98-U99, ISSN: 1359-6535
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- Citations: 1
Kantor R, Carvalho AP, Wynhoven B, et al., 2003, Nucleic acid differences between HIV-1 non-B and B reverse transcriptase and protease sequences at drug resistance positions, 12th International HIV Drug Resistance Workshop, Publisher: INT MEDICAL PRESS LTD, Pages: U58-U59, ISSN: 1359-6535
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- Citations: 7
Price DA, Scullard G, Oxenius A, et al., 2003, Discordant outcomes following failure of antiretroviral therapy are associated with substantial differences in human immunodeficiency virus-specific cellular immunity, JOURNAL OF VIROLOGY, Vol: 77, Pages: 6041-6049, ISSN: 0022-538X
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- Citations: 25
Cozzi-Lepri A, Phillips AN, Miller V, et al., 2003, Changes in viral load in people with virological failure who remain on the same HAART regimen, ANTIVIRAL THERAPY, Vol: 8, Pages: 127-136, ISSN: 1359-6535
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- Citations: 22
Igakura T, Stinchcombe JC, Goon PKC, et al., 2003, Spread of HTLV-I between lymphocytes by virus-induced polarization of the cytoskeleton, SCIENCE, Vol: 299, Pages: 1713-1716, ISSN: 0036-8075
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- Citations: 547
Igakura T, Stinchcombe JC, Goon PK, et al., 2003, HTLV-I spreads between lymphocytes by virus-induced polarization of the cytoskeleton., 11th International Conference on Human Retrovirology: HTLV and Related Viruses, Publisher: MARY ANN LIEBERT INC PUBL, Pages: S15-S15, ISSN: 0889-2229
Taylor GP, Goon P, Usuku K, et al., 2003, The bridge study - A double-blind placebo controlled trial of zidovudine plus lamivudine for treatment of patients with HTLV-I-associated myelopathy., 11th International Conference on Human Retrovirology: HTLV and Related Viruses, Publisher: MARY ANN LIEBERT INC PUBL, Pages: S13-S14, ISSN: 0889-2229
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- Citations: 2
Myint L, Ariyoshi K, Yan H, et al., 2002, Mutagenically separated PCR assay for rapid detection of M41L and K70R zidovudine resistance mutations in CRFO1_AE (Subtype E) human immunodeficiency virus type, ANTIMICROBIAL AGENTS AND CHEMOTHERAPY, Vol: 46, Pages: 3861-3868, ISSN: 0066-4804
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- Citations: 11
Oxenius A, Price DA, Dawson SJ, et al., 2002, Residual HIV-specific CD4 and CD8 T cell frequencies after prolonged antiretroviral therapy reflect pretreatment plasma virus load, AIDS, Vol: 16, Pages: 2317-2322, ISSN: 0269-9370
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- Citations: 21
Fidler S, Oxenius A, Brady M, et al., 2002, Virological and immunological effects of short-course antiretroviral therapy in primary HIV infection, AIDS, Vol: 16, Pages: 2049-2054, ISSN: 0269-9370
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- Citations: 49
Walmsley S, Bernstein B, King M, et al., 2002, Lopinavir-ritonavir versus nelfinavir for the initial treatment of HIV infection., N Engl J Med, Vol: 346, Pages: 2039-2046
BACKGROUND: Lopinavir is a newly developed inhibitor of human immunodeficiency virus (HIV) protease that, when formulated with ritonavir, yields mean trough plasma lopinavir concentrations that are at least 75 times as high as that needed to inhibit replication of wild-type HIV by 50 percent. METHODS: We conducted a double-blind trial in which 653 HIV-infected adults who had not received antiretroviral therapy for more than 14 days were randomly assigned to receive either lopinavir-ritonavir (400 mg of lopinavir plus 100 mg of ritonavir twice daily) with nelfinavir placebo or nelfinavir (750 mg three times daily) with lopinavir-ritonavir placebo. All patients also received open-label stavudine and lamivudine. The primary efficacy end points were the presence of fewer than 400 HIV RNA copies per milliliter of plasma at week 24 and the time to the loss of virologic response through week 48. RESULTS: At week 48, greater proportions of patients treated with lopinavir-ritonavir than of patients treated with nelfinavir had fewer than 400 copies of HIV RNA per milliliter (75 percent vs. 63 percent, P<0.001) and fewer than 50 copies per milliliter (67 percent vs. 52 percent, P<0.001). The time to the loss of virologic response was greater in the lopinavir-ritonavir group than in the nelfinavir group (hazard ratio, 2.0; 95 percent confidence interval, 1.5 to 2.7; P<0.001). The estimated proportion of patients with a persistent virologic response through week 48 was 84 percent for patients receiving lopinavir-ritonavir and 66 percent for those receiving nelfinavir. Both regimens were well tolerated, with the rate of discontinuation related to the study drugs at 3.4 percent among patients receiving lopinavir-ritonavir and 3.7 percent among patients receiving nelfinavir. Among patients with more than 400 copies of HIV RNA per milliliter at some point from week 24 through week 48, resistance mutations in HIV protease were demonstrated in viral isolates from 25 of 76 nel
Frater AJ, Dunn DT, Beardall AJ, et al., 2002, Comparative response of African HIV-1-infected individuals to highly active antiretroviral therapy, AIDS, Vol: 16, Pages: 1139-1146, ISSN: 0269-9370
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- Citations: 104
Lindenburg CEA, Stolte I, Langendam MW, et al., 2002, Long-term follow-up:: no effect of therapeutic vaccination with HIV-1 p17/p24:Ty virus-like particles on HIV-1 disease progression, VACCINE, Vol: 20, Pages: 2343-2347, ISSN: 0264-410X
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- Citations: 32
Frater J, Dunn D, Weber JN, et al., 2002, Association between secondary mutations in human immunodeficiency virus type 1 protease and therapeutic outcome, JOURNAL OF INFECTIOUS DISEASES, Vol: 185, Pages: 1376-1376, ISSN: 0022-1899
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- Citations: 6
Kaleebu P, French N, Mahe C, et al., 2002, Effect of human immunodeficiency virus (HIV) type 1 envelope subtypes A and D on disease progression in a large cohort of HIV-1-positive persons in Uganda, JOURNAL OF INFECTIOUS DISEASES, Vol: 185, Pages: 1244-1250, ISSN: 0022-1899
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- Citations: 193
Goon PKC, Hanon E, Igakura T, et al., 2002, High frequencies of Th1-type CD4<SUP>+</SUP> T cells specific to HTLV-1 Env and Tax proteins in patients with HTLV-1-associated myelopathy/tropical spastic paraparesis, BLOOD, Vol: 99, Pages: 3335-3341, ISSN: 0006-4971
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- Citations: 75
Kaye S, Dunn DT, Babiker AG, et al., 2002, Observations of HIV-1 genotypic drug resistance in a trial of four reverse transcriptase inhibitors (Quattro Trial), ANTIVIRAL THERAPY, Vol: 7, Pages: 11-20, ISSN: 1359-6535
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- Citations: 4
Mocroft A, Phillips AN, Friis-Møller N, et al., 2002, Response to antiretroviral therapy among patients exposed to three classes of antiretrovirals: results from the EuroSIDA study., Antivir Ther, Vol: 7, Pages: 21-30, ISSN: 1359-6535
There is an increasing proportion of HIV-positive patients exposed to all licensed classes of antiretrovirals, and the response to salvage regimens may be poor. Among over 8500 patients in EuroSIDA, the proportion of treated patients exposed to nucleosides, protease inhibitors (PIs) and non-nucleoside reverse transcriptase inhibitor (NNRTI) increased from 0% in 1996 to 47% in 2001. Four-hundred-and-thirteen patients, who had failed virologically two highly active antiretroviral therapy (HAART) regimens and experienced all three main drug classes, started a salvage regimen of at least three drugs, in which at least one new PI or NNRTI was included. Median viral load was 4.7 log copies/ml [Interquartile range (IQR) 4.2-5.2], CD4 lymphocyte count 150/mm3 (IQR 60-274/mm3) and follow-up 14 months. Of these patients, 283 (69%) subsequently experienced at least a 1 log decline in viral load and 202 (49%) achieved a viral load < 500 copies/ml. Conversely, the CD4 count halved from the baseline value in 88 (21%), and 45 (11%) experienced a new AIDS-defining disease. In multivariable analyses, a 1 log viral load reduction was related to baseline viral load [relative hazard (RH) 1.27 per 1 log higher; P = 0.008], a previous viral load of less than 500 copies/ml (RH 1.69; P = 0.002), more recent initiation of the regimen (RH 1.36 per year more recent; P = 0.02), number of new drugs in the regimen (RH 1.20 per drug; P = 0.02), time since start of antiretroviral therapy (RH 0.94 per extra year; P = 0.035) and time spent on HAART with viral load > 1000 copies/ml (RH 0.96 per extra month; P = 0.0001). Analysis of factors associated with CD4 count decline and new AIDS disease also indicated improved outcomes in more recent times and a tendency for a better response in those starting more new drugs, but no relationship with the total number of drugs. Outcomes in people starting salvage regimens appear to depend on the number of new drugs started but not on the total number of d
Riabov GS, Kazennova EV, Korepanova LB, et al., 2002, [The HIV-infection outbreak in the town Lys'va (Perm region): homozygote genotype CCR5 delta32/CCR5 delta32 provides the high level of the persistence in the parenteral transmission of the virus]., Vopr Virusol, Vol: 47, Pages: 13-16, ISSN: 0507-4088
Specific features of human immunodeficiency virus type 1 (HIV-1) transmission among injecting drug users were studied on HIV infection outbreak in Lysva, the Perm region. During the period from November 1998 to March 2000, 32 injecting drug users infected with the subtype A HIV-1 variant originating from the same source, were found in this town. To understand the role of the CCR5 delta 32 mutation in parenteral transmission of HIV-1 the distribution of the mutant CCR5 delta 32 allele in HIV-infected and in non-infected but HIV-exposed drug users (n = 74) was analysed. The percentage of the homozygous CCR5 delta 32 genotype among HIV-exposed individuals (4/74, 5.4%) was significantly (p < 0.05) higher than the analogous rate for healthy blood donors in Russia (1/163, 0.6%). Thus, the homozygosity for this mutant allele confers a high resistance level to HIV even in parenteral transmission.
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