Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Parenteral drug abusers are at risk for acquired immunodeficiency syndrome (AIDS), which is caused by human immunodeficiency virus (HIV). We tested stored sera for antibody to HIV (anti-HIV) using two enzyme-linked immunosorbent assay (ELISA) methods and Western blot. The patients were parenteral drug abusers who had undergone percutaneous liver biopsy for chronic liver disease. Current or former alcohol abuse was noted in 88 (80%) of the 110 patients. The sensitivities of the two ELISA tests in comparison with Western blot, the more specific test for HIV, were 100 and 94%, respectively; the specificities were 94 and 99%. Western blot was positive in 36 (33%) of 110 patients. False-positive ELISA reactions for anti-HIV were seen in five (7%) of 70 patients with negative Western blot analyses. Compared to true-negatives, false-positives had significantly more years of alcohol abuse, younger ages of onset of alcohol abuse, greater frequencies of jaundice and edema, higher levels of alkaline phosphatase, total billirubin, total protein, and globulins, and lower levels of serum albumin. In a stepwise logistic regression, only hyperglobulinemia was significantly associated with a false-positive anti-HIV. We conclude that: (a) ELISA tests for anti-HIV are useful for screening abusers of alcohol and parenteral drugs with chronic liver disease for HIV infection, but positive results must be confirmed with more specific tests such as Western blot; (b) false-positive ELISA reactions in this population are associated with hyperglobulinemia; and (c) studies of HIV testing are needed in other populations of patients with alcoholism or liver disease.
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PMID:Specificity of antibody tests for human immunodeficiency virus in alcohol and parenteral drug abusers with chronic liver disease. 306 17

Four patients with acquired immunodeficiency syndrome (AIDS) (CDC group IV) were investigated for biliary disease because of the presence of both severe upper abdominal pain and raised levels of serum alkaline phosphatase. None was clinically jaundiced. Upper abdominal ultrasound was abnormal in three. All had endoscopic retrograde cholangiographic evidence of both an intrahepatic sclerosing cholangitis suggestive of primary sclerosing cholangitis and an irregular suprapapillary common bile duct dilation suggestive of papillary stenosis. Three had evidence of gastrointestinal cryptosporidiosis and two of disseminated cytomegalovirus infection. Endoscopic sphincterotomy, performed in two patients, gave good pain relief. We propose the name 'AIDS sclerosing cholangitis' for this form of secondary cholangitis. The cause of this disorder remains unclear. Recent evidence is discussed which suggests that it is not due to HIV itself but to an opportunistic infection. Cryptosporidium appears to be the most likely candidate.
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PMID:Sclerosing cholangitis in acquired immunodeficiency syndrome. Case reports and review of the literature. 307 60

Adherent human embryo brain cells have been infected with HIV. Cells replicating HIV were maintained in culture for seven sequential passes over 7 months and continued to produce HIV during that time. Human embryo brain cells displayed glial-cell morphology and expressed glial fibrillary acidic protein. Electron microscopy showed clusters of virus particles around these cells as well as budding virus. Extracted, infected glial cells revealed bands for three major gag proteins, p18, p24 and p55, in Western blotting. It was not possible to detect CD4 antigen on the surface of these cells by indirect immunofluorescence or alkaline phosphatase staining with CD4 monoclonal antibodies. The results of these experiments indicate that HIV replicates in non-malignant brain cells. This observation strengthens the postulated aetiological link between HIV and the encephalopathy, dementia and other neurological symptoms observed in HIV-infected patients.
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PMID:HIV replicates in cultured human brain cells. 312 70

Up to 30% of patients with acquired immunodeficiency syndrome (AIDS) suffer from Kaposi's sarcoma (AIDS-KS). The histogenesis and neoplastic nature of this tumor is still controversial. We have established cell cultures of KS biopsies from 7 patients with AIDS. All donors were seropositive for the human immunodeficiency virus I (HIV-I), cytomegalovirus (CMV) and hepatitis B virus (HBV). The tumors were histologically shown to be KS. Cell cultures derived from these tumors all expressed the endothelial cell marker BMA 120 antigen. Most of these cultures were positive for acetylated low-density lipoprotein (acLDL) uptake and alkaline phosphatase (AP) expression, and negative for factor-VIII-related antigen (FVIII-RAg). The staining pattern was heterogeneous with respect to number of endothelial cell markers expressed in each culture. We conclude from subcloning experiments that the cultured cells cease to express acLDL receptor and AP, but not the antigen detected by the monoclonal antibody (MAb) BMA 120. The cells grew well in culture up to 50 passages and showed a fibroblast-like morphology. Assays performed to investigate their degree of malignancy revealed a significantly increased passage number under reduced serum conditions as compared to normal fibroblasts but no tumor formation in nude mice. Neither HIV, HBV nor CMV sequences were found in any of the cell lines tested. We conclude that AIDS-KS is an endothelial-cell-derived neoplasm of low malignancy and that HIV, HBV and CMV are not directly involved in its genesis.
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PMID:Cultured, AIDS-related Kaposi's sarcoma cells express endothelial cell markers and are weakly malignant in vitro. 314 Dec 99

Plasmids were constructed whereby the expression of a reporter gene, either the cDNA corresponding to the secreted form of human alkaline phosphatase (SEAP) or the herpes simplex virus type 1 (HSV1) thymidine kinase (tk) gene, was rendered dependent upon the expression of the human immunodeficiency virus type 1 (HIV1) tat and rev proteins. The SEAP or tk genes were placed between HIV1 splice donor and acceptor sites. One SEAP construct carried a series of alternating splice donor and acceptor sites. In all cases, the rev response element mapped within an intron. Despite such mimicry of the HIV1 genome, residual expression of the reporter gene in the absence of tat and rev was observed. These results, as well as non-specific T-cell recruitment, suggest limits to the specificity of using HIV-activated toxic gene expression to kill HIV-infected cells.
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PMID:Residual expression of reporter genes in constructs mimicking HIV genome organization. 748 Oct 89

Monoclonal antibodies (MAbs) were raised against the gag protein of human immunodeficiency virus type 1 (HIV-1). The reactivity of the selected Mabs with the matrix protein p17 of HIV-1 were investigated in several tests, i.e. ELISA, immunostaining of Western blots, and alkaline phosphatase anti-alkaline phosphatase immunocytochemistry (APAAP). All three Mabs reacted exclusively with HIV-1 and showed specific binding to the virus surface in pre-embedding immuno-electron-microscopy and useful as diagnostic agents. In an "in vitro" cultivation experiment the MAbs showed antiviral activity in concentrations in the range of 25-100 micrograms/ml. No binding region could be defined using overlapping peptides consisting of the p17 protein sequence of HIV-1 in an epitope mapping system and therefore we concluded, that the MAbs recognize a conformational epitope.
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PMID:Characterization of murine monoclonal antibodies directed against the submembrane protein p17 of HIV-1. 750 41

We studied two monoclonal antibodies (MAbs 9-11 and 41-1) which are specific for dominant and conserved epitopes located on HIV-1 transmembrane Gp41. These MAbs recognize both Gp41 and a synthetic HIV-1 envelope peptide (39GC) which is a fragment of Gp41. The interactions between MAbs 9-11 and 41-1 and 39GC either coupled to a sensor chip or to alkaline phosphatase were investigated using BIAcore technology. The association and dissociation rate constants as well as the affinity constants were determined. BIAcore technology allows real-time determination of the interaction between two molecules without the need for any labeling, neither isotopic nor enzymatic. The peptide 39GC was immobilized by coupling to dextran on the BIAcore biosensor through a disulfide bond with a cysteine residue added to the N-terminus of the synthetic peptide. The two native cysteine residues located in the loop of Gp41 were protected by ethylcarbamoyl residues (CONHC2H5); this chemical modification prevented the formation of the S-S bridge and in particular the internal loop. We specifically studied the interaction between the MAbs and either the protected peptide or the peptide whose cysteine residues had been deprotected in situ by alkaline treatment. The results showed that MAb 41-1 recognized 39GC either protected (Ka = 7.6 x 10(6) M-1) or unprotected (Ka = 1.48 x 10(8) M-1), whereas MAb 9-11 recognized only the unprotected form (Ka = 2.18 x 10(8) M-1). Our results suggest that the epitope MAb 9-11 is directed against a part of the peptide sequence which includes the two native cysteines. The difference in affinity observed for MAb 41-1 between the protected and the unprotected forms of 39GC was found to be due to a lower rate of dissociation for unprotected 39GC; these results illustrate the importance of peptide conformation on antibody recognition and might be explained by a conformational change due to reconstitution of the internal loop following deprotection of the thiol groups. MAbs 9-11 and 41-1 also recognized 39GC conjugated to alkaline phosphatase and deprotected. We observed a difference between the rate constants for MAb 41-1 binding to free peptide and its binding to the peptide-enzyme conjugate which might be due to changes in peptide flexibility. In contrast, the rate constants of MAb 9-11 were the same in both experiments, suggesting that the rigidity of the internal loop prevents changes in 9-11 epitope conformation.
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PMID:Effect of HIV-1 peptide presentation on the affinity constants of two monoclonal antibodies determined by BIAcore technology. 751 68

An epitope from the HIV-1 gp120 protein V3 loop has been inserted onto the surface of bacterial alkaline phosphatase at different positions in the vicinity of the enzyme active site, creating hybrid proteins that can bind to an anti-gp120 monoclonal antibody. One of the hybrid proteins, API1, has a 13 amino acid V3 loop sequence inserted between residues 407 and 408 of alkaline phosphatase. The enzymatic activity of this protein is modulated upon antibody binding. API1 maintains the full activity of the wild type alkaline phosphatase but in the presence of the anti-gp120 antibody, the enzyme activity is inhibited by 40-50%. Thus, the hybrid enzyme can be used to detect the presence of antibody in solution. The concept of signalling proteins may have a wide application. Two models for the mechanism of modulation, steric hindrance and allosteric regulation, are discussed.
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PMID:Modulation of enzyme activity by antibody binding to an alkaline phosphatase-epitope hybrid protein. 751 83

An enzyme-linked immunosorbent assay (ELISA) using biotin-labelled oligo-dT primer and digoxigenin (Dig)-dUTP was designed to measure the reverse transcriptase (RT) activity of human immunodeficiency virus type 1 (HIV-1). The ELISA system involves the selective detection step of a newly synthesized cDNA by two specific bindings, biotin-streptavidin binding and alkaline phosphatase (AP)-conjugated anti-Dig-Dig binding, and the enzymatic amplification step to increase coloring generated by AP. This method was used to measure the activity of RT in the culture supernatants of peripheral leukocytes obtained from four anti-HIV-1-positive persons cocultivated with those from four anti-HIV-1-negative persons. RT activity was detected in all of four anti-HIV-1-positive culture supernatants but not in those cultivated with anti-HIV-1-negative supernatants alone. Thus, our improved ELISA for detection of HIV-1 appears to be sensitive enough and useful for routine laboratory work. This non-radioactive method will also be useful for detecting other retroviruses and for screening of RT inhibitors.
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PMID:Detection of reverse transcriptase activity by enzyme-linked immunosorbent assay in human immunodeficiency virus type 1. 754 28

We retrospectively analysed 46 cases of disseminated infection with Mycobacterium avium complex (MAC) within a cohort of 702 HIV-infected patients in Edinburgh. Clinical features were compared with case-matched controls (AIDS cases without disseminated MAC), and survival and progression times were controlled for confounding variables that influence survival. Disseminated MAC was diagnosed antemortem in 18% of AIDS patients, and was the AIDS-defining diagnosis in 6% of all AIDS cases. Concomitant colonization of respiratory and gastrointestinal tracts was common (61% and 48%, respectively). In 58% of cases, CD4+ counts were < 10 cells/mm3 (median 6 cells/mm3). Weight loss, anaemia, leucopenia, and elevated liver transaminases and alkaline phosphatase were significantly more common among cases than controls. Therapy was given in 74%, and not tolerated in 32%. Following AIDS diagnosis, disseminated MAC incidence was 14% at one year, 25% at 2 years and 36% at 3 years. Median survival after disseminated MAC diagnosis was 6 months, with shorter survival in untreated cases. However, overall survival from AIDS diagnosis was not significantly different between patients who did or did not develop disseminated MAC. Disseminated MAC contributes significantly to AIDS morbidity, and its incidence increases with prolonged AIDS survival. Although survival following diagnosis is short, the development of disseminated MAC in AIDS probably does not affect overall survival. In cohorts with a low incidence, an alternative to prophylaxis might be surveillance and early diagnosis.
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PMID:Disseminated disease due to Mycobacterium avium complex in AIDS. 758 75


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