Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0021051 (immunodeficiency)
71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eight Belgian AIDS Reference Laboratories established a multicentre quality control to evaluate the performance of their diagnostic human immunodeficiency virus type 1 (HIV-1) DNA polymerase chain reaction (PCR). A set of Belgian and African HIV-1 seropositive and seronegative patient samples, collected in Belgium, and the British Medical Research Council (MRC) HIV-1 PCR reference reagent kit, containing plasmid HIV-1 DNA at several dilutions in human carrier DNA with appropriate negative controls, were tested by the laboratories. No false positive results were reported. All laboratories were able to detect one to two copies of HIV-1 DNA. Among the 17 Belgian and African HIV-1 seropositives, some laboratories reported up to four indeterminate results, mainly due to failure of the SK38-39, SK68-69 (Ou et al. (1988) Science 239, 295-297) and/or gag881-882 (Simmonds et al. (1990) J. Virol. 64, 864-872) primers and a poorly performing algorithm. Only the H1POL4235-4538 nested pol primer set, developed by one of the laboratories, correctly identified all the tested HIV-1 positive and negative samples. Consequently, the laboratories decided to evaluate these pol primers as a reference primer set and to standardise the testing algorithm. All laboratories achieved a sensitivity and specificity of 100% on testing 10 additional Belgian and African patient samples, when adapting a standardised algorithm based on three HIV-1 primer sets, one of which is the H1POL4235-4538 primer set.
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PMID:Standardisation of primers and an algorithm for HIV-1 diagnostic PCR evaluated in patients harbouring strains of diverse geographical origin. The Belgian AIDS Reference Laboratories. 773 51

The efficiency of detection of 2 sets of primer pairs from putatively conserved regions of the human immunodeficiency virus type 2 (HIV-2) genome were assessed in 86 seropositive individuals from The Gambia by nested polymerase chain reaction (PCR). HIV-2 long terminal repeat (LTR) target sequences were detected in DNA extracted from peripheral blood mononuclear cells (PBMCs) in 84 of 86 (97%) individuals whereas HIV-2 integrase (pol) gene sequences were detected in 39 of 41 (95%) individuals. The use of LTR target sequences and recombinant Pfu DNA polymerase, rather than Taq polymerase, in a modified secondary amplification reaction mediated the incorporation of 35S-labeled nucleotides in a quantitative radiometric assay. This sensitive assay was used to quantify HIV-2 proviral DNA in clinical samples and compared well with estimations by limiting end-point dilution of target molecules. A linear response between counts and the number of copies amplified from serial dilutions of pROD10 plasmid DNA (3-2000 copies) yielded a standard curve to allow extrapolation to clinical data. Increased levels of HIV-2 proviral DNA, expressed as copies per 10(5) CD4-positive lymphocytes, were associated with declining CD4 count in 63 adult patients (Spearman rank correlation, r = -0.71, n = 63, p < 0.001) and with the occurrence of HIV-related clinical disease. Kruskall-Wallis analysis of variance analysis showed the mean proviral copy number (log10) to be significantly different between groups (p < 0.001) where CD4 counts were grouped as < 200/mm3 (3.4 +/- 1.05 copies), 200-500/mm3 (2.84 +/- 0.93 copies), and > 500/mm3 (1.88 +/- 0.43 copies).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:HIV type 2 proviral load measured by quantitative polymerase chain reaction correlates with CD4+ lymphopenia in HIV type 2-infected individuals. 781 34

Serum specimens (n = 161) from 31 persons before and after human immunodeficiency virus type 1 (HIV-1) seroconversion were tested for anti-CD4 antibodies. These antibodies were detected by both ELISA and Western blot in 55% (17/31) of subjects when HIV-1 seroconversion was detected and in 26% (8/31) from sera obtained 6-24 months earlier. A decrease in CD4+ cell number was associated more with development of anti-CD4 antibodies or peak anti-CD4 antibody activity than with development of anti-HIV-1 antibodies. Quantitative DNA polymerase chain reaction assay of peripheral blood mononuclear cells from 7 seroconverters showed evidence of HIV-1 infection in 4 of 4 specimens obtained after HIV-1 seroconversion but was nonreactive for 12 of 12 specimens obtained before HIV-1 seroconversion, including 4 specimens positive for anti-CD4 antibodies by ELISA and Western blot. Therefore, anti-CD4 antibodies are frequently present in the sera of HIV-1-infected persons before and at the time HIV-1 seroconversion is detectable and are associated with a decline in CD4+ cell counts, but they are not a marker for HIV-1 infection in seronegative persons.
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PMID:Association between anti-CD4 antibodies and a decline in CD4+ lymphocytes in human immunodeficiency virus type 1 seroconverters. 784 66

Measurements of human immunodeficiency virus by quantitative RNA and DNA polymerase chain reaction (PCR), cell and plasma infectivity dilution cultures, and immune complex-disassociated p24 antigen-capture ELISA were made repeatedly in 10 subjects receiving long-term zidovudine treatment before and after therapy was changed to didanosine. Comparison of baseline assays showed that quantitative cell cultures, plasma RNA, and proviral DNA were measurable in all subjects and that cell culture results were significantly correlated with measures of nucleic acids. Plasma viremia (as indicated by culture) and p24 antigen were detected in three measurements in 3 of 8 and 6 of 10 subjects, respectively. Significant decreases in plasma RNA and cell dilution cultures from baseline were maintained for up to 6 months after initiation of didanosine therapy. These findings demonstrate a decrease in virus burden with the use of didanosine; however, continued detection of plasma RNA suggests that additional antiviral therapy will be required to suppress viral replication.
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PMID:Quantitation of human immunodeficiency virus by culture and polymerase chain reaction in response to didanosine after long-term therapy with zidovudine. 790 92

To evaluate the prognostic value of provirus copy number through quantitative DNA polymerase chain reaction (PCR) in early stages of human immunodeficiency virus type 1 (HIV-1) infection, 42 untreated and asymptomatic HIV-1-seropositive subjects with baseline CD4+ cell counts > 200 x 10(6)/L were included in a prospective study and followed over a median of 27 months. Disease progression was defined as decrease in CD4+ cells to < 200 (14 events). At enrollment, provirus copy number was associated with CD4+ cell count and percentage, serum IgA, and p24 antigenemia. Elevated provirus copy number above 20 allowed identification of patients at high risk of a subsequently decreasing CD4+ cell count, even after adjusting for baseline CD4+ cell count (P = .003). Measuring provirus copy number by PCR at early stages of HIV-1 infection could offer a useful early means to predict progression to AIDS.
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PMID:Provirus copy number to predict disease progression in asymptomatic human immunodeficiency virus type 1 infection. 790 43

The purpose of this study was to characterize quantitative changes in circulating infected cells over the natural history of human immunodeficiency virus (HIV) disease in relation to clinical/immunological outcome. HIV-1 gag DNA polymerase chain reaction (PCR) and peripheral blood mononuclear cell (PBMC) co-cultures were performed on limiting dilutions of cryopreserved PBMC from specimens collected at enrollment and after 5 years of follow-up from nine seropositive subjects classified as rapid progressors, nine intermediate progressors, and 10 nonprogressors. Limiting dilution PCR was also performed on serial pre/postseroconversion specimens from 18 seroconvertors. By quantitative DNA PCR analysis, the infected cell burden was significantly higher at enrollment in the RP [mean of 330 PCR units (PCRU)/10(6) PBMCs] than in the IP (160 PCRU/10(6) PBMCs) and NP (73 PCRU/10(6) PBMCs) groups (p = 0.05). When results were analyzed on an individual level with proportional hazard regression, baseline PCRU (p = 0.05) and CD4 slope (p = 0.0007) were significantly associated with developing acquired immune deficiency syndrome (AIDS) in 5 years, but baseline tissue culture infectious units (TCIU) was not. The increase in PCR-positive cells after 5 years was modest in all three groups (two- to fivefold), whereas the proportion of PCR-positive cells that yielded virus in culture increased significantly (21- to 31-fold) over time in all three groups. Infected cell burden in postseroconversion specimens was relatively stable within each subject, but varied greatly (from 1.6 to 1,024 PCRU/10(6) PBMCs) among subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Circulating HIV-1-infected cell burden from seroconversion to AIDS: importance of postseroconversion viral load on disease course. 790 63

The safety and efficacy of combined therapy with polyethylene glycolated (PEG) interleukin (IL)-2 and zidovudine was assessed in 19 human immunodeficiency virus type 1 (HIV-1)-seropositive subjects in a phase I/II open-label dose-ranging study. During courses of three weekly infusions of PEG IL-2, dose-limiting side effects were seen at 5 x 10(6) IU/m2 and reversible encephalopathy in 1 subject at 3 x 10(6) IU/m2. Significant increases were seen in CD4 cell counts (P < .01), NK cell activity (P < .05), and HIV-specific cytotoxicity (P < .01). Virologic monitoring (quantitative DNA polymerase chain reaction and p24 antigen assay) showed no evidence of increased HIV activation. Patients with CD4 cells < 200/mm3 were entered into a chronic dosing phase. PEG IL-2 was given at 14-day intervals at doses of 10(6) IU/m2 for 8 weeks and 3 x 10(6) IU/m2 for up to 16 weeks, resulting in mean CD4 cell count elevations of 16% and 33%, respectively. PEG IL-2 appears to warrant further investigation, especially in subjects with CD4 cell counts < 200/mm3, to determine whether increased lymphocyte numbers will translate into improved clinical outcome.
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PMID:Safety and efficacy of polyethylene glycol-modified interleukin-2 and zidovudine in human immunodeficiency virus type 1 infection: a phase I/II study. 809 58

A method for quantitating human immunodeficiency virus type 1 plasma viremia may be useful in monitoring disease progression and the responsiveness of patients to a therapeutic regimen or vaccine. A quantitative assay for viral RNA in plasma or sera that differs in several aspects from those reported previously was developed. First, whereas conventional reverse transcriptase-PCR assays involve a two-step process and use two enzymes, the method described uses a single enzyme, rTth DNA polymerase, for both reverse transcription and PCR. The reactions are carried out in a single tube and with a single buffer solution with uninterrupted thermal cycling. Second, uracil-N-glycosylase and dUTP are incorporated into the reaction mixtures to ensure that any carryover of DNA from previous amplifications will not compromise quantitation. Third, a quantitation standard is incorporated into each reaction mixture so that differences in amplification efficiency caused by sample interferents, variability in reaction conditions, or thermal cycling can be normalized. To ensure comparable amplification efficiency, the quantitation standard has the same primer-binding regions as the human immunodeficiency virus type 1 target and generates an amplified product of the same size and base composition. The probe-binding region was replaced with a sequence that can be detected separately. Fourth, a colorimetric detection format was modified to provide at least a four-log-unit dynamic range. The quantitative assay requires only a single amplification of the sample and can be completed in less than 8 h. The procedure was used on archival samples to demonstrate the viremic spike in acute infection and the suppressed levels of circulating virus following seroconversion.
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PMID:Rapid and simple PCR assay for quantitation of human immunodeficiency virus type 1 RNA in plasma: application to acute retroviral infection. 815 Sep 37

The human immunodeficiency virus (HIV), the human T cell lymphotropic virus (HTLV-1), the human foamy retrovirus and the simian immunodeficiency viruses have been associated with the development of an inflammatory myopathy in humans and primates. The myopathy caused by HIV and HTLV-1 is not due to direct infection of the muscle by these viruses, but rather due to an immunopathologic process triggered by the viruses, mediated by autoaggressive CD8+ cells in the context of MHC-class I antigen expression. This has been based on a series of studies utilizing immunocytochemistry, in situ hybridization, polymerase chain reaction, and co-cultivation of human myotubes with the viruses or with HIV-1 and HTLV-1-infected homologous lymphoid cells. Because the clinical, histological and immunological picture of patients with retroviral-associated inflammatory myopathies is identical to that of patients with retroviral-negative inflammatory myopathy, there is a reasonable possibility that retroviruses may be candidate viruses in triggering inflammatory myopathies. In recent years, the antiretroviral drug AZT (Zidovudine), commonly used for the treatment of AIDS, has been shown to cause a distinct mitochondrial myopathy characterized by depletion of the muscle mitochondrial DNA due to AZT's ability to inhibit the gamma-DNA polymerase of the mitochondrial matrix. Distinction of the AZT-myopathy is clinically important because it responds to discontinuation of AZT and to administration of another antiretroviral agent such as ddI or ddC.
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PMID:Retroviruses and inflammatory myopathies in humans and primates. 815 47

Triple helices can be formed on single-stranded oligopurine target sequences by composite oligonucleotides consisting of two oligonucleotides covalently linked by either a hexaethylene glycol linker or an oligonucleotide sequence. The first oligomer forms Watson-Crick base pairs with the target, while the second oligomer engages in Hoogsteen base pairing, thereby acting as a molecular clamp. The triple-helical complex formed by such an oligonucleotide clamp, or "oligonucleotide-loop-oligonucleotide" (OLO), is more stable than either the corresponding trimolecular triple helix or the double helix formed upon binding of the oligopyrimidine complement to the same oligopurine target. Attaching a psoralen derivative to the 5' end of the OLO allowed us to photoinduce a covalent linkage to the target sequence. The psoralen moiety became covalently linked to all three portions of the triplex, thereby making the oligonucleotide clamp irreversible. These crosslinking reactions introduced strong stop signals during DNA replication, as shown on a plasmid containing a portion of the HIV proviral sequence of human immunodeficiency virus. A 16-mer oligopurine sequence corresponding to the "polypurine tract" of human immunodeficiency virus was chosen as a target for a psoralen-OLO conjugate. Three different stop signals for DNA polymerase were observed, corresponding to different sites of polymerase arrest on its template. Even in the absence of photoinduced crosslinking, the psoralen-OLO conjugate was able to arrest DNA replication. The formation of triple-helical structures on single-stranded targets may provide an alternative to the antisense strategy for the control of gene expression.
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PMID:Oligonucleotide clamps arrest DNA synthesis on a single-stranded DNA target. 823 49


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