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)

The transcription factor HIV-TF1, which binds to a region about 60 bp upstream from the enhancer of the human immunodeficiency virus-1 (HIV-1), was purified from human B cells. HIV-TF1 had a molecular weight of 39,000. Binding of HIV-TF1 to the HIV long terminal repeat (LTR) activated transcription from the HIV promoter in vitro. The HIV-TF1-binding site in HIV LTR was similar to the site recognized by upstream stimulatory factor (USF) in the adenovirus major late promoter. DNA-binding properties of HIV-TF1 suggested that HIV-TF1 might be identical or related to USF. Interestingly, treatment of purified HIV-TF1 by phosphatase greatly reduced its DNA-binding activity, suggesting that phosphorylation of HIV-TF1 was essential for DNA binding. The disruption of HIV-TF1-binding site induced a 60% decrease in the level of transcription from the HIV promoter in vivo. These results suggest that HIV-TF1 is involved in transcriptional regulation of HIV-1.
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PMID:USF-related transcription factor, HIV-TF1, stimulates transcription of human immunodeficiency virus-1. 165 50

In 34 patients with human immunodeficiency virus (HIV) infection at the asymptomatic stage and 29 patients with chronic viral hepatitis B at the period of exacerbation (of these 14 patients had chronic persistent hepatitis and 15 patients had chronic active hepatitis) the complex study of the functional activity of lymphocytes and neutrophils was carried out by cytochemical methods with the simultaneous determination of the content of immunoregulating lymphocyte subpopulations. In patients with chronic active hepatitis a decrease in the percentage and the absolute number of helper T-lymphocytes and the ratio of CD4/8 in comparison with those in patients with HIV infection were revealed. At the same time patients with HIV infection exhibited more pronounced decrease in the activity of all lymphocytic enzymes under study (neutrophil esterase, acidic phosphatase and succinate dehydrogenase in lymphocytes), as well as in the activity of myeloperoxidase and the content of cation proteins and glycogen in neutrophils in comparison with patients having chronic active hepatitis.
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PMID:[The comparative characteristics of the indices of lymphocyte and neutrophil functional activity in patients with HIV infection and chronic viral hepatitis B]. 167 92

We have used a specific phosphatase inhibitor, okadaic acid, to examine the role of two phosphatases, PP1 and PP2A, in the induction of NF-kappa B and the long terminal repeat of the human immunodeficiency virus type 1 (HIV-LTR). Treatment of Jurkat cells with okadaic acid induced NF-kappa B in nuclear extracts. The rate of induction by okadaic acid was delayed compared to the induction of NF-kappa B by phorbol myristate acetate (PMA). The induction of NF-kappa B by okadaic acid was enhanced by cycloheximide or phytohemagglutinin (PHA). In contrast to PMA, okadaic acid appeared to induce NF-kappa B independently of protein kinase C (PKC). That the NF-kappa B induced by okadaic acid was functional was demonstrated by the marked increase in CAT activity that occurred in Jurkat, BJA-B, and U251 cells that were transfected with HIV-LTR-CAT and treated with okadaic acid. The increase in CAT activity triggered by okadaic acid was dependent on the presence of the NF-kappa B sites in the long terminal repeat of HIV as assessed by deletion and mutation analysis. Similarly to its effect on the induction of NF-kappa B, PHA added together with okadaic acid resulted in a further increase in CAT activity. Somewhat surprisingly, the addition of PMA inhibited the increase in CAT activity in response to okadaic acid, which suggests that the activation of PKC may also induce inhibitory factors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Induction of nuclear factor-kappa B and the human immunodeficiency virus long terminal repeat by okadaic acid, a specific inhibitor of phosphatases 1 and 2A. 217 54

Thirty four patients positive for human immunodeficiency virus (HIV) who had lymphadenopathy were investigated using fine needle aspiration. Cytological analysis included immunocytochemical investigation with the alkaline phosphatase-antialkaline phosphatase (APAAP) method. All patients had confirmation of cytological diagnosis by lymph node biopsy. Fifteen aspirates with follicular hyperplasia were evaluated. Eleven patients showed B cell predominance. The B cell population did not show light chain restriction. Ten patients with B cell non-Hodgkin's lymphoma (five with Burkitt's lymphoma and five with B cell immunoblastic lymphoma) were investigated. Nine out of 10 cases were monoclonal with respect to their light chain determinants; only one case with Burkitt's lymphoma with partial lymph node metastasis did not show light chain restriction. The cytological diagnosis included two mycobacterial infections and four cystic lesions. Histological investigation was necessary to diagnose the extent of lymph node disease caused by Kaposi's sarcoma. These findings indicate that the immunocytological investigation of lymph node aspirates is useful for evaluating lymphadenopathy in HIV positive patients.
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PMID:Immunocytochemical analysis of lymph node aspirates in patients with human immunodeficiency virus infection. 222 33

The nucleoside analog 2',3'-dideoxycytidine (ddCyd) has been shown to inhibit the infectivity and cytopathic effect of human immunodeficiency virus on human OKT4+ lymphocytes in vitro. Metabolism of ddCyd by human T-lymphoblastic cells (Molt 4) negative for human immunodeficiency virus and OKT4 was examined. Molt 4 cells accumulated ddCyd and its phosphorylated derivatives into acid-soluble and acid-insoluble material in a dose-dependent manner. For each concentration tested, 2',3'-dideoxycytidine triphosphate represented 40% of the total acid-soluble pool of ddCyd metabolites. Uptake of 5 microM ddCyd was linear for 4 h after addition of drug. Efflux of ddCyd metabolites from cells followed a biphasic course with an initial retention half-life of 2.6 h for 2',3'-dideoxycytidine triphosphate. DNA, but not RNA, of cells incubated with [3H]ddCyd became radiolabeled. Nuclease and phosphatase treatment of DNA followed by reverse-phase high pressure liquid chromatography showed that the nucleoside was incorporated into DNA in its original form. ddCyd was not susceptible to deamination by human Cyd-dCyd deaminase. It was a poor substrate for human cytoplasmic and mitochondrial dCyd kinases, with Km values of 180 +/- 30 and 120 +/- 20 microM, respectively. DNA polymerases alpha, beta, and gamma varied in their sensitivity to inhibition by ddCTP with Ki values of 110 +/- 40, 2.6 +/- 0.3, and 0.016 +/- 0.008 microM, respectively; however, inhibition was competitive with dCTP in each case.
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PMID:Cellular metabolism of 2',3'-dideoxycytidine, a compound active against human immunodeficiency virus in vitro. 243 80

The enhancer element of the human immunodeficiency virus type I (HIV-I) long terminal repeat (LTR) contains two copies of nearly identical sequences AGGGACTTTCC (3G sequence) and GGGGACTTTCC (4G sequence) that are important in transcriptional regulation. A single copy of the 4G sequence is found in the NF-kappa B site of the immunoglobulin kappa-chain enhancer. Only the 4G motif in the HIV enhancer is bound by cellular proteins in extracts prepared from unstimulated HeLa cells, whereas the 3G and 4G motifs are bound by factors in extracts prepared from HeLa cells treated with phorbol esters [phorbol 12-myristate 13-acetate (PMA)] and lymphoid cells. To determine if this change in binding to the HIV enhancer was due to phosphorylation of a cellular protein, partially purified PMA-treated HeLa nuclear extracts were digested with calf intestinal phosphatase. Phosphatase digestion of nuclear extracts from PMA-treated HeLa cells markedly decreased factor binding to the HIV enhancer. Accordingly, phosphorylation of the DNA binding protein itself, or an inhibitor protein present in the partially purified extract, must mediate binding to the recognition sequence. Binding studies confirmed that each of the enhancer sequences was capable of binding factors independent of the activity of the other site and that the HIV enhancer was occupied by only one factor at any one time. Chloramphenicol acetyltransferase assays using mutants in either one or both HIV enhancer repeats revealed that each site was capable of functioning as a tat-inducible enhancer element in PMA-treated HeLa cells. These results suggest that the 3G and 4G motifs in the HIV enhancer function independently and that duplication in the HIV enhancer augments activity by a mechanism distinct from cooperative binding of NF-kappa B.
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PMID:Repeated B motifs in the human immunodeficiency virus type I long terminal repeat enhancer region do not exhibit cooperative factor binding. 320 Aug 27

The authors describe 4 families whose members showed myeloproliferative diseases. In one of the families, polycythemia vera (PV) was seen in twin brother and sister, in the other one, chronic myeloleukemia (CML) afflicted both daughter and mother, and in the two remaining families PV and CML afflicted two brothers and mother and daughter, respectively. It was established that neutrophil phosphatase activity was lowered not only in the afflicted brother but also in healthy members of the third family. Based on the reported and their own data the authors arrive at the conclusion that familial myeloproliferative diseases occur in rare cases. In all the cases of familial myeloproliferative diseases, the transmission of the illness by heredity was discovered to be impossible. It was also ascertained that transmitted by heredity are only those cell deficiencies of the tissues that later on will be afflicted by leukemia or will develop immunodeficiency manifested by increased mutation of the myelopoietic cells (DNA repair deficiencies) or by inability to eliminate the leukemic cells.
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PMID:[Familial myeloproliferative syndrome (study of 4 families and review of the literature)]. 386 57

A significant cholestasis constellation (alk. phosphatase and GGT each increased to twice as much as the norm) in 73 consecutive patients with AIDS was found in the course of the disease in 29 patients (= 39.7%). In most of the patients advanced immunodeficiency with an average of 2.5 AIDS-defining diseases already existed. In the predominant number of cases it was intrahepatic cholestasis with only slight icterus. Therapeutic measures such as medicamentous treatment or high-caloric parenteral nutrition were causal in two thirds of the cases; in a quarter of the cases opportunistic infections, above all disseminating mycobacteriosis were found. One third of the patients had already existing liver diseases. Liver biopsy frequently proved diagnostic and should be performed more often in the case of unclear liver findings in AIDS patients.
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PMID:[Incidence and differential diagnosis of cholestasis in AIDS--a retrospective analysis of 73 patients]. 748 95

Gastrointestinal and biliary abnormalities are common in the acquired immunodeficiency syndrome. Although obviously related to opportunistic infections in many cases, often no infectious agent can be identified. The specific diagnosis depends on invasive methods such as endoscopic retrograde cholangiography and liver histology. To evaluate an alternative and less invasive first-line approach, we conducted a prospective study of microscopic examination of aspirated duodenal/bile juice, to try to identify microbial causes of human immunodeficiency virus (HIV)-related gastrointestinal and biliary tract disease. Sixty-four HIV-infected patients underwent upper gastrointestinal endoscopy with biopsies from the esophagus, stomach, and duodenum, and aspiration of stimulated duodenal/bile juice. Biopsies, duodenal/bile juice, and stool samples were examined for enteric pathogens. Twenty-seven intestinal infections were found in 22 of the 64 patients (34%), 12 (44%) of which were diagnosed by duodenal/bile juice examination. Seven of the 27 infections (26%) were diagnosed exclusively in duodenal/bile juice, whereas 5 were found in biopsies or stool samples as well. Twenty infections (74%) were demonstrated in intestinal biopsies and/or stool samples, 15 without any positive result in duodenal/bile juice. The proportion of patients with elevated alkaline-phosphatase and gamma-glutamyl-transpeptidase activities was higher in patients with infectious agents detected in duodenal/bile juice (5 of 11, 45%), than in patients with infectious agents found exclusively in intestinal biopsies and/or stool samples (2 of 11, 18%). Analysis of duodenal/bile juice is a simple, rapid, and effective method for the detection of enteral pathogens in HIV-related gastrointestinal and biliary dysfunction. It increases the diagnostic yield above the results of intestinal biopsies and stool examinations alone.
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PMID:Stimulated duodenal/bile juice aspiration for diagnosis of enteric pathogens in HIV-infected patients. 756 Aug 31

Motheaten viable (mev) mice are deficient in the cytosolic protein tyrosine phosphatase, PTP1C, and exhibit severe B cell immunodeficiency and autoantibody production. The role of PTP1C in B cell selection and function was analyzed by breeding immunoglobulin transgenes specific for a defined antigen, hen egg lysozyme, into mev mice. Antigen triggered a greater and more rapid elevation of intracellular calcium in PTP1C-deficient B cells, indicating that this phosphatase negatively regulates immunoglobulin signaling. Elimination of self-reactive B cells carrying this signal-enhancing mutation was triggered during their development by binding a lower valency form of self-antigen than is normally required. These findings establish that activation of distinct repertoire-censoring mechanisms depends on quantitative differences in antigen receptor signaling, whose thresholds are determined by negative regulation through PTP1C.
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PMID:Protein tyrosine phosphatase 1C negatively regulates antigen receptor signaling in B lymphocytes and determines thresholds for negative selection. 760 Feb 99


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