Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.5.4.4 (adenosine deaminase)
 5,136 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There are now rather straightforward methods to create transgenic animals whose genome is altered at the germline level. One method consists in the micro-injection of a gene into the pronucleus of a fertilized egg, the second one involves an homologous recombination event obtained in embryonic stem cells in culture. Only the latter method could eventually lead to an authentic gene therapy since it could actually substitute a normal gene for a mutated one instead of merely introducing a supplementary gene as done by micro-injection. Description of these techniques makes it obvious that germline therapy of human beings would not only be inacceptable on ethical grounds but would also hardly have any medical indications. Quite on the contrary, somatic gene therapy does not suffer from the same reservations and has numerous potential applications to man. As a matter of fact, several protocols have already received approval and have reached the stage of clinical trials: for example SCID (severe combined immunodeficiency due to a mutated adenosine deaminase gene), AIDS as well as some forms of malignant tumors.
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PMID:[Transgenesis and gene therapy]. 130 2

Evidence of an acquired T cell-specific deficiency distinct from acquired immunodeficiency syndrome (AIDS) in a 63-yr-old Japanese female is provided. Recently, this patients suffered from primary invasive pulmonary aspergillosis. Skin tests to purified protein derivative of tuberculin (PPD) and Aspergillus antigens were negative. Upon admission to our hospital, her lymphocytes were exclusively unresponsive to T cell mitogens (concanavalin A, phytohemagglutinin, and OKT 3). The level of cells defined by monoclonal antibodies (CD1, CD2, CD3, CD4, WT31, and CD5) was less than 3%. In contrast, no decrease in the number of red blood cells, platelets, neutrophils or B cells was apparent. Five years ago, the patient had a normal white blood cell and lymphocyte count. However, over the following 4 yr, she developed lymphopenia. With medication, her pulmonary disease recovered, while lymphopenia still continued. The levels of immunoglobulins, complements and enzyme activities (adenosine deaminase and purine nucleoside phosphorylase) were normal. Moreover, several tests for HIV (ELISA and Western bolt) were negative suggesting that the T cell-specific deficiency was not a congenital immunodeficiency or AIDS but rather a new type of acquired immunodeficiency.
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PMID:Acquired T cell specific deficiency other than acquired immunodeficiency syndrome (AIDS). 156 29

The value of ascites gamma interferon concentration and ascites adenosine deaminase activity in distinguishing tuberculosis from other causes of ascites was examined in a prospective study of 86 patients with ascites, including 16 with tuberculous peritonitis. Gamma interferon concentration was higher in tuberculous peritonitis than in the other causes of ascites (p less than 0.0001), and a cut-off between 3 and 9 u/ml reached a sensitivity and a specificity of 100%. The mean (+/- SD) gamma interferon level in tuberculous ascites was 39.3 +/- 18.3 u/ml in patients seronegative for HIV and 14.2 +/- 4.7 u/ml in patients with AIDS (p = 0.01). Adenosine deaminase activity in tuberculous ascites was also higher than in the other causes of ascites (p less than 0.0001), and a cut-off of 40 u/l reached a sensitivity of 100% and a specificity of 97%. The two false positives for adenosine deaminase test were true negatives for the gamma interferon test. There was no significant correlation between gamma interferon concentration and adenosine deaminase activity either in tuberculous ascitis or in any other group. This study suggests that ascites gamma interferon determination may be very useful in the screening of tuberculous peritonitis, but its cost makes it advisable to use adenosine deaminase activity as a routine test, at least in areas where tuberculosis is endemic.
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PMID:Diagnostic value of ascites gamma interferon levels in tuberculous peritonitis. Comparison with adenosine deaminase activity. 177 79

The levels of adenosine deaminase (ADA) were determined in the erythrocytes of 10 patients with sexually transmitted HIV-1 infection [five cases with AIDS-related complex (ARC) and five with AIDS] before and after therapy with zidovudine (azidothymidine; AZT). A linear increase in ADA activity was observed during the second and third months of zidovudine treatment, with a final increase of about threefold after 3 months of drug administration. The concentration of adenosine triphosphate (ATP) was significantly lower in the erythrocytes of the same group of patients with respect to healthy controls, and a further decrease was noted after 3 months of zidovudine treatment. The results obtained indicate that treatment of ARC/AIDS subjects with zidovudine induces metabolic changes which could be responsible for the development of anaemia, an adverse effect frequently associated with zidovudine therapy.
AIDS 1990 Aug
PMID:Enhancement of erythrocytic adenosine deaminase following treatment of AIDS-related complex/AIDS patients with zidovudine. 226 Nov 34

(+-) Carbocyclic 2',3'-didehydro-2',3'-dideoxyguanosine (Carbovir; NSC 614846) is an antiretroviral agent which is undergoing preclinical evaluation for the treatment of AIDS. Racemic carbovir was separated into its D and L enantiomers by the action of adenosine deaminase on the 2,6-diaminopurine precursor. Subsequent evaluation of the enantiomers against human immunodeficiency virus type 1 revealed that the antiviral activity of carbovir resides in the (-) isomer that is analogous to the nucleoside, beta-D-2',3'-didehydro-2',3'-dideoxyguanosine.
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PMID:Resolution of racemic carbovir and selective inhibition of human immunodeficiency virus by the (-) enantiomer. 234 92

Enzyme activities were studied in peripheral blood lymphocytes from patients infected with, or at risk for, infection with human immunodeficiency virus (HIV). No significant differences were observed in the HIV-infected and HIV-seronegative high-risk patients with regard to enzyme activities of hypoxanthine-guanine phosphoribosyltransferase (EC 2.4.2.8) and purine nucleoside phosphorylase (EC 2.4.2.1) in peripheral blood. Adenosine deaminase (EC 3.5.4.4) was significantly (P less than 0.02) depressed in asymptomatic HIV-seropositive patients and HIV-seronegative patients at high risk of HIV infection as compared with a healthy HIV-seronegative population. Adenosine kinase (AK, EC 2.7.1.20) was significantly increased in the asymptomatic seropositive (P less than 0.02) and also in the HIV-seronegative high-risk groups (P = 0.01) compared with the normal controls. AK activity was significantly lower in subjects with AIDS than in the asymptomatic (P less than 0.002) and high-risk groups (P less than 0.01). Taken together, these results indicate that adenosine deaminase and AK activities are influenced by the health of the patient, and that measurement of AK activity may prove useful in monitoring the clinical progress of patients with HIV infection.
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PMID:Depressed activities of purine enzymes in lymphocytes of patients infected with human immunodeficiency virus. 254 31

The levels of purine enzyme activities were studied in 10 patients with acquired immunodeficiency syndrome (AIDS) or AIDS related complex (ARC) and in 6 healthy individuals with antibodies against human immunodeficiency virus (HIV). All AIDS/ARC patients studied had ecto-5'nucleotidase (ecto-5'NUC) activity in B lymphocytes below the normal range and 4 out of 6 clinically healthy HIV-positive likewise had reduced activity. Increased numbers of activated B lymphocytes were found both in the group of healthy HIV positive individuals and in AIDS/ARC patients. Further studies are needed to define whether the decrease in ecto-5'NUC activity on the B lymphocytes is a result of increased activation of the cells or of a B cell defect. No significant changes were found in ecto-5'NUC levels in T lymphocytes or mononuclear cells (MNC), neither in the group of AIDS/ARC patients nor in the healthy HIV-positive group. Both AIDS/ARC patients and healthy individuals with antibodies against HIV had increased levels of adenosine deaminase (ADA) activity in mononuclear cells, but only in the group of AIDS/ARC patients was the increase significant. No changes were found in purine nucleoside phosphorylase (PNP) activity in the two groups tested. From these investigations of purine enzyme levels and other markers of immune function in both sick and healthy HIV infected individuals we conclude that the observed changes in ecto-5'NUC and ADA activities in HIV infected patients are not a direct result of the HIV infection but develop early in the course of the disease.
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PMID:Decreased B lymphocyte ecto-5'nucleotidase and increased adenosine deaminase in mononuclear cells from patients infected with human immunodeficiency virus. 284 68

"Immune regulation: what immunodeficiency disease has taught us" is reviewed by discussing three immuno-deficiency disorders. Hypogammaglobulinemia, the first documented primary immunodeficiency disorder, has a well defined and uniform clinical presentation which reflects a variety of underlying abnormalities involving the B cell, T cell, and monocyte. X-linked hypogammaglobulinemia, transient hypogammaglobulinemia of infancy common variable immunodeficiency, and their pathogenesis are discussed. Combined immunodeficiency with adenosine deaminase (ADA) deficiency first led to the now accepted concept that a biochemical abnormality may result in immunodeficiency. The clinical presentation, possible biochemical abnormalities resulting in the observed immunodeficiency, relative selectivity of the defect for the immune system, and potential applications of knowledge gained from the study of ADA deficiency are presented. Acquired immunodeficiency (AIDS) has resulted in the concept that a virus is cytopathic for a specific population of T cells and that this, at least in part, results in the immunodeficiency seen in AIDS.
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PMID:Immune regulation: what immunodeficiency disease has taught us. 298 76

Thymosin fraction 5 (Thymosin) has numerous immunoregulatory activities including modulation of enzymes involved in lymphocyte maturation. The effect of Thymosin on the purine metabolic enzymes adenosine deaminase (ADA), purine nucleoside phosphorylase (PNP), and 5' nucleotidase (5'NT) in null and T-enriched peripheral blood lymphocytes from sexually active asymptomatic homosexual males (AS), patients with the AIDS-related symptom complex (ARC), and those with acquired immune deficiency syndrome (AIDS) was examined and compared to its effect on lymphocytes from healthy heterosexual controls. Mean ADA activity was significantly higher in null cells from fourteen AIDS patients than in five asymptomatic homosexuals, ten ARC patients, or 27 controls. Mean PNP activity was significantly elevated in null-enriched lymphocytes from ten ARC and fourteen AIDS patients compared to controls. No differences in these enzymes were found in T-enriched cells from any group. 5'NT was markedly decreased in both null and T lymphocytes in all homosexual groups relative to controls. Homosexuals had significantly elevated percentages of OKT10 positive and Ia positive lymphocytes compared to controls. Thymosin at an optimal concentration of 150 micrograms/ml caused significant decreases in mean ADA and PNP activity in null lymphocytes from ARC + AIDS patients along with a significant decrease in the percentage of OKT10 positive lymphocytes. No phenotypic changes were seen in AS or control lymphocytes. The data suggest that Thymosin has a maturational effect in vitro on immature T cells from symptomatic homosexuals.
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PMID:In vitro modulation of purine enzyme metabolism and lymphocyte surface marker expression by thymosin fraction 5 in homosexual males. 299 64

The classification of the pediatric acquired immunodeficiency syndrome (AIDS) is based on epidemiologic, immunologic, and virologic data. Persons at risk include mothers who use intravenous drugs, infants who have received blood transfusions from subjects with risk factors, patients receiving factor VIII therapy, and infants born to heterosexual mothers with bisexual husbands. A distinct immunologic phenotype, rarely seen in other immunodeficiency disorders, is associated with pediatric AIDS consisting of polyclonal hypergammaglobulinemia and T-cell immunodeficiency. Detection of antibody to the AIDS retrovirus or isolation of virus are essential in establishing a diagnosis. During early infancy, viral isolation is essential as passive transfer of material IgG may occur. Primary immunodeficiency diseases, in particular adenosine deaminase and purine nucleoside phosphorylase deficiency, should be excluded. A diagnosis of pediatric AIDS may be established in a patient who has a risk factor associated with AIDS, polyclonal hypergammaglobulinemia, T-cell immunodeficiency, and antibody to the AIDS retrovirus or isolation of virus.
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PMID:The acquired immunodeficiency syndrome in infants and children. 299 9


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