UMLS:C0019693 - FACTA Search

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Query: UMLS:C0019693 (HIV)
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In 1994, hepatitis C virus (HCV) infection was transmitted to four HIV seropositive patients attending the Department of Angiology, University Clinics, Frankfurt am Main, by the administration of Gammagard. The patients were suffering from thrombocytopenia and received betweeen 20 and 30 g of the contaminated lot 93F21AB11. GBV-C/HGV RNA could be amplified from the Gammagard lot 93F21AB11 using 5'NCR and NS5 primer pairs. All the four patients were negative in the GBV-C/HGV RT-PCR prior to therapy and until the end of the follow-up period. GBV-C/HGV IgG antibodies to the putative envelope (E2) were detected using the E2 HGV-env kit (Boehringer-Mannheim, Germany) in Gammagard lot 93F21AB11 and in one patient before donation of immunoglobulin. Anti-E2 seroconversion was observed in one recipient, the other two patients remained anti-E2 seronegative until the end of the observation period. It is concluded that there is no direct evidence for transmission of GBV-C/HGV by contaminated intravenous immunoglobulin since GBV-C/HGV RNA was not detected in the recipients up to 1 year after administration.
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PMID:Follow-up of four HIV-infected individuals after administration of hepatitis C virus and GBV-C/hepatitis G virus contaminated intravenous immunoglobulin: evidence for HCV but not for GBV-C/HGV transmission. 929 28

HIV infection in humans causes various aberrancies in both the cellular and humoral immune systems, including functional abnormalities of B lymphocytes. In many instances, dysfunction occurs in the regulation of serum IgA, resulting in elevated concentrations of this immunoglobulin isotype. To determine whether HIV-1-infected chimpanzees develop IgA abnormalities similar to those observed in humans, we quantified total IgA, IgG, and IgM levels in sera collected longitudinally from six HIV-infected chimpanzees and one uninfected control animal. In comparison to immunoglobulin levels in the uninfected animal, two of the six infected chimpanzees exhibited increases in serum immunoglobulins following infection with HIV. Two other infected animals showed a marked decrease in the three isotypes within 10 months of exposure to HIV, followed by a return to baseline levels. The remaining two HIV-infected chimpanzees displayed serum immunoglobulin levels that paralleled the baseline levels and did not show great deviation over a period of 20 to 45 months postinfection. ELISA analyses of the IgA subclasses revealed possible abnormalities of the IgA2 subclass within the two animals that did not display irregular IgA, IgG, or IgM responses to HIV-1. Specific IgG, IgA, IgA1, and IgA2 antibodies to HIV antigens were detected by an enzyme immunoassay (EIA) kit and by Western blot analysis with IgA, IgA1, and IgA2 antibodies directed against the env, gag, and pol gene products. Because IgG can mask the detection of HIV-specific IgA antibodies in infected humans, Western blots and EIAs were also performed on IgG-depleted chimpanzee sera. The results demonstrated that in some instances, IgA reactivity against HIV antigens can be enhanced on removal of IgG. This study indicates that HIV-1 is capable of inducing abnormalities in serum IgA expression in chimpanzees. These results might further understanding of how HIV affects humoral responses in infected humans.
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PMID:IgA immunity in HIV type 1-infected chimpanzees. I. Systemic immunity. 933 43

Total antioxidant capacity (TAC) of fasting EDTA plasma of 33 healthy and 64 HIV-infected patients was determined using H(2)O(2)-peroxidase-ABTS technique. The results revealed that the average TAC in HIV-infected patients was significantly lower than those in healthy normal persons. (0.161 +/- 0.097 vs 0.269 +/- 0.081 mmol/L Trolox equivalent, p < 0.05). Total lymphocytes were also counted using Hycel automatic cell counter and absolute CD4 numbers using Coulter CD4 manual kit. It was interesting that CD4 count was not correlated with the clinical symptoms of the patients. This paper suggests that prediction of severity and monitoring of the disease should be performed by determining both total lymphocyte count and total antioxidant capacity.
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PMID:Total antioxidant capacity in plasma of HIV-infected patients. 934 58

The purpose of this review is to give an update of the recent progress in research on erythropoietin (Epo), the hormone that regulates red blood cell production. Epo is a glycoprotein with a molecular mass of approx 30 kDa, which circulates in plasma of the human with 165 amino acids with three N-linked and one O-linked acidic oligosaccharide side chains in the molecule. Both the alpha (39% CHO) and beta (24% CHO) forms are available for clinical use, and there does not appear to be any difference in the pharmacokinetics of these two forms of Epo. Radioimmunoassays and enzyme-linked immunoabsorbant (ELISA) assays are available in a kit form. Serum levels of Epo in normal human subjects range between 1 and 27 mmu/ml or approx 5 pmol/l. It seems clear that the cells in the adult mammalian kidney which produce Epo are the interstitial cells in the peritubular capillary bed and the perivenous hepatocytes in the liver. Expression of the human Epo gene sequences that direct expression in the kidney are located 6-14 kilobases 5' to the gene; whereas the sequences that control hepatocyte-specific expression are located within 0.7 KS to the 3'-flanking region and 0.5 KS to the 5'-flanking region. The signal transduction pathways postulated to be involved in the expression of Epo are: kinases A, G and C; both a constitutive factor and a second hypoxia-inducible factor-1 (HIF-1) located in the 5' end of an hypoxia inducible enhancer region of the Epo gene; and reactive oxygen species. The primary target cell in the bone marrow acted on by Epo is the colony-forming unit erythroid (CFU-E) which has the highest number of Epo receptors. It has been postulated that Epo decreases the rate which Epo-dependent progenitor cells undergo programed cell death (apoptosis). There are two major signal transduction pathways activated by the Epo receptor: the JAK2-STAT5 pathway and the ras pathway. Both pathways involve tyrosine phosphorylation. The approved clinical uses of Epo are the anemias associated with end-stage renal disease, cancer chemotherapeutic agents, and patients with HIV infection receiving AZT. Other anemias reported to respond to Epo therapy are anemia of prematurity, rheumatoid arthritis, and myelodysplasia. Other uses of Epo under investigation are in perioperative surgery and preoperative autologous blood donation.
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PMID:Erythropoietin: physiologic and pharmacologic aspects. 940 40

The immune complex transfer enzyme immunoassays for antibody IgGs to p17, p24, and reverse transcriptase (RT) of HIV-1 were tested under various conditions. Antibody IgGs to HIV-1 were reacted for up to 20 hr with 2,4-dinitrophenyl-bovine serum albumin-recombinant HIV-1 protein conjugates and recombinant HIV-1 protein-beta-D-galactosidase conjugates, and the immune complexes formed, comprising the three components, were trapped onto polystyrene beads coated with (anti-2,4-dinitrophenyl group) IgG by incubation at 4-30 degrees C for up to 2 hr with shaking and were transferred onto polystyrene beads coated with (antihuman IgG gamma-chain) IgG in the presence of excess of epsilon N-2,4-dinitrophenyl-L-lysine by incubation at 4-30 degrees C for up to 2 hr with shaking. When serum randomly collected from an HIV-1 seropositive subject and serum included in an Western blot kit were tested, the formation of the immune complex was almost completed within 1 hr for antibody IgG to p17, within 1-2 hr for antibody IgG to p24 and within 4 hr for antibody IgG to RT. Even for antibody IgG to p17, however, the immune complex continued to be formed for at least 2 hr, when serum samples at early stages of HIV-1 infection were tested. Trapping and transferring of the immune complexes were faster at higher temperatures and were almost completed within 0.5-1.5 hr, although the amount of the immune complexes trapped and transferred at 25 and/or 30 degrees C increased for 0.5-1 hr, but subsequently tended to decline. When the formation, trapping, and transferring of the immune complexes were performed for 0.5, 1, and 1 hr, respectively, with shaking followed by 1 hr assay of bound beta-D-galactosidase activity, the sensitivities for antibody IgGs to p17, p24, and RT using 10 microliters of serum samples were similar to or significantly higher than those of the corresponding previous immune complex transfer enzyme immunoassays using 10 microliters of serum samples, in which the formation, trapping, and transferring of the immune complexes were performed for 3, 16, and 3 hr, respectively, without shaking, followed by 2.5 hr assay of bound beta-D-galactosidase activity, and the sensitivities for antibody IgGs to p17, p24, and RT using 100 microliters of serum samples were 21-22-fold, 5.5-6.3-fold, and 5.3-6.0-fold, respectively, higher. When each period of time for the formation, trapping, and transferring of the immune complexes was prolonged to up to 4 hr, the sensitivities for antibody IgGs to p17, p24, and RT using 100 microliters of serum samples were improved 88-93-fold, 15-17 fold and 20-24-fold, respectively, as compared with those of the previous ones.
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PMID:Optimal conditions of immune complex transfer enzyme immunoassays for antibody IgGs to HIV-1 using recombinant p17, p24, and reverse transcriptase as antigens. 952 94

Our objectives were to estimate the cost per syringe distributed for five syringe distribution strategies (a needle exchange program [NEP], a pharmacy-based NEP, free pharmacy distribution of pharmacy kits, sale of such pharmacy kits to injection drug users [IDUs], and sale of syringes in pharmacies); to assess the total costs of these strategies; and to conduct an economic analysis of these strategies in preventing HIV infection in IDUs. We estimated the costs for NEPs by using data from previous research; costs for the four pharmacy-based strategies were resource-based. Using estimates of the number of syringes required to provide a sterile syringe for each IDU injection, we estimated the total costs of the strategies in three representative U.S. cities. The lifetime cost of treating a person for HIV infection, discounted into current value, was used to estimate the number of syringes that could be distributed for that amount by the five strategies and thus the number of IDUs who could be ensured a sterile syringe for each injection. We then conducted a threshold analysis for calculating the annual HIV seroincidence for the program to be cost-neutral. The cost per syringe distributed in U.S. dollars was $0.97 for the NEP, $0.37 for the pharmacy-based NEP, $0.64 for pharmacy kit distribution, $0.43 for pharmacy kit sale, and $0.15 for syringe sale. The total annual cost in U.S. dollars of providing 50% of the syringes needed for a single syringe for every injection ranged from $6 to $40 million for New York City, from $1 to $6 million for San Francisco, and from $30,000 to $200,000 for Dayton, Ohio. The annual HIV seroincidence for the program to be cost-neutral compared with the cost of medical treatment for HIV injections was 2.1% for the NEP, 0.8% for the pharmacy NEP, 1.4% for pharmacy kit distribution, 0.9% for pharmacy kit sale, and 0.3% for syringe sale. All five strategies could distribute syringes at relatively low unit costs; NEPs would be the most expensive and syringe sales would be the cheapest. At annual seroincidences exceeding 2.1%, all strategies are likely to be cost-saving to society.
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PMID:An economic analysis of needle exchange and pharmacy-based programs to increase sterile syringe availability for injection drug users. 966 35

False negativity in a commercial anti-HIV kit (IMx HIV-1/HIV-2 3rd Generation Plus (code 8B32) was investigated, and the kit that superseded it (IMx HIV-1/HIV-2 III Plus, code 8C98) was evaluated. In a comparison on 574 freshly collected anti-HIV-1-positive specimens, 97.2% were more reactive in 8C98 than in 8B32; 35.5% were more than twice as reactive and 8.5% were more than four times as reactive. In 8B32, the signal from 55 specimens selected because of weak reactivity was enhanced 1.5 to 8.8 times by preliminary heating at 56 degrees C for 30 min. The reactivity of the 55 heated sera was then similar to that of the same specimens tested without heat treatment in the 8C98 assay. Reactivity in 8B32 was also increased in 66 of 76 (at least twofold in 20) randomly chosen anti-HIV-positive serum specimens by the addition of EDTA (10 mM final concentration). One of these specimens was false negative (signal:cutoff (S:CO) ratio 0.76) in 8B32, though its reactivity was restored by addition of EDTA (S:CO ratio 9.54). These findings indicate that the inhibitory effect that originally led to false negative findings in 8B32 was probably due to complement activity, and that the same activity was present in the freshly collected specimens used here to evaluate the replacement IMx anti-HIV assay (8C98). The specimen panel employed to evaluate 8C98 included 1,892 anti-HIV-positive and 779 anti-HIV-negative specimens. There were no false negative reactions. The lowest S:CO ratio observed was 6.2 and only 17 (0.2%) anti-HIV-positive specimens gave ratios less than 10. Nine unreproducible false positive reactions arose, all possibly attributable to specimen carryover by the IMx instrument. The performance of 8C98 was also compared with that of 10 other current anti-HIV kits using 21 sets of seroconversion specimens (127 specimens in total), and five performance assessment panels (92 specimens in total) comprised mostly of single bleeds from recent seroconverters. IMx 8C98 was the second most sensitive assay. We found no evidence that the 8C98 kit was prone to the effect that had given rise to false negative results in its predecessor (8B32).
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PMID:False negativity by an anti-HIV assay kit (IMx 8B32) and evaluation of its replacement (IMx 8C98). 974 70

This study addresses the limited range of quantification with colorimetric assays (ELISA) starting from the analysis of color production in a reference external curve. An automatic ELISA management software, designated Quanti-Kin Detection System (QKDS) is described, which retains the sensitivity of the end-point reading and extends the dynamic range up to five logarithms with mathematical interpretation of color production. The QKDS software is a generic system suitable for different types of ELISA with substrate incubation at room temperature, does not require dedicated instruments, performs accurate quantification (including assay quality control) and has a user friendly interface. Specific applications were developed for three types of analytes: antibodies, viral antigens and nucleic acids. Data are presented on three representative QKDS applications to HIV antibodies, p24 antigen and proviral DNA kits. The precision of quantification is strictly correlated with the precision of the kit; however, for almost all samples with known analyte amount, the error percentage was below 10%, only for two cases in quantification of HIV proviral DNA the error percentage was around 25%. The necessity for a wide quantification range has been demonstrated by measuring clinical samples, which showed a distribution in all possible quantification ranges for all kits.
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PMID:A novel and innovative quantitative kinetic software for virological colorimetric assays. 976 91

Enzyme immunoassay is the basic method for the detection of antibodies to the Human Immunodeficiency Virus (HIV). In spite of the apparent facility of the serological screening, the difficulties are real at all stages of the analysis. Specimen treatment needs defined rules to avoid contamination. The products authorized are listed by the "French Drug Agency". The specificity cannot be less than 99.5%, and the sensitivity must be of 100%. Each biologist have to acquire its own experience of the tests utilised. To the very recent seroconversions, he must define decision criteria for the pursuit or not of the investigations. False positive have been observed for patients with autoimmune pathology, but was usually related to a disparity between kit lots.
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PMID:[Topicality of serologic screening of human immunodeficiency virus infections in adults]. 976 38

Procedures for quality control (QC) in a laboratory that concentrates on cytokine and soluble marker measurements in biological fluids are outlined. Intra-assay, interassay, and interlaboratory experiences are presented. Plasma and serum beta2-microglobulin (beta2M) and neopterin test data are presented in greatest detail, along with substantial tumor necrosis factor alpha (TNF-alpha), gamma interferon, soluble interleukin-2 receptor-alpha (sIL-2Ralpha), sTNF-RII, IL-4, and IL-6 data. Recommended QC procedures for cytokine and soluble-marker testing include replicate testing of two or more reference samples provided by the kit manufacturer, replicate testing of in-house frozen reference QC samples that represent normal and abnormal analyte contents, retesting 15 to 20% of randomly selected samples, and comparing normal reference ranges each year. Also, eight cytokines and soluble markers were evaluated in human immunodeficiency virus (HIV)-seronegative and HIV-seropositive individuals stratified on the basis of CD4 T-cell numbers. Levels of some but not all cytokines in serum increased in HIV infection. There was a tendency for cytokines to increase with more advanced disease, defined by reduced CD4 T-cell numbers. Cytokine changes did not relate closely to CD4 level, indicating that separate information was provided by the measurements of TNF-alpha, sTNF-RII, sIL-2Ralpha, beta2M, and neopterin. Serum IL-4 and TNF-alpha levels were not increased. The quality of laboratory data can impact on clinical relevance. Interlaboratory comparisons revealed substantial differences at some sites and documented the need for external proficiency-testing quality assurance programs.
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PMID:Levels of cytokines and immune activation markers in plasma in human immunodeficiency virus infection: quality control procedures. 980 30

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