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 absence of erythrocytic adenosine deaminase (ADA) or purine nucleoside phosphorylase (PNP) has been associated with severe immunodeficiency disease in children. We have developed a cell culture model to study the possible relationships between purine salvage enzymes and immunologic function using an established T cell lymphosarcoma (S49) and a potent inhibitor of ADA, erythro-9(2-hydroxy-3-nonyl) adenine (EHNA). Wild-type S49 cells are killed by dexamethasone or dbc AMP, and adenosine (5 muM) in the presence of an ADA inhibitor (6 muM EHNA) also prevents the growth of and kills these S49 cells. It has been proposed that adenosine is toxic to lymphoid cells by virtue of its ability to increase the intracellular concentrations of cyclic AMP. We examined the sensitivity of three mutants of S49 cells, with distinctive defects in some component of cyclic AMP metabolism or action, to killing by adenosine and EHNA. All three mutants are resistant to killing by isoproterenol or cholera toxin and two are resistant to dbc AMP itself, but all are sensitive to killing by adenosine and EHNA. Similarly, two dexamethasone-resistant S49 mutants are as sensitive to adenosine and EHNA as are the wildtype cells. We have also simulated the purine nucleoside phosphorylase deficiency in S49 cells by adding inosine and adenosine to the growth medium. In the presence of EHNA or inosine, the toxic effects of adenosine can be partially reversed by addition of (10-20 muM) uridine, an observation suggesting that adenosine is toxic as the result of its inducing pyrimidine starvation.
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PMID:Characterization of a cell culture model for the study of adenosine deaminase- and purine nucleoside phosphorylase-deficient immunologic disease. 18 61

One of the most important aspects of preparing travelers for destinations throughout the world is providing them with immunizations. Before administering any vaccines, however, a careful health and immunization history and travel itinerary should be obtained in order to determine vaccine indications and contraindications. There are three categories of immunizations for foreign travel. The first category includes immunizations which are routinely recommended whether or not the individual is traveling. Many travelers are due for primary vaccination or boosting against tetanus-diphtheria, measles-mumps-rubella, pneumococcal pneumonia, and influenza, for example, and the pre-travel visit is an ideal time to administer these. The second category are immunizations which might be required by a country as a condition for entry; these are yellow fever and cholera. The final category contains immunizations which are recommended because there is a risk of acquiring a particular disease during travel. Typhoid fever, meningococcal disease, rabies, and hepatitis are some examples. Travelers who are pregnant or who are infected with the human immunodeficiency virus require special consideration. Provision of appropriate immunizations for foreign travel is an important aspect of preventing illness in travelers.
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PMID:Immunizations for foreign travel. 133 7

WHO statistics indicated that as of October 1, 1991 there were 418,403 acquired immunodeficiency syndrome (AIDS) patients in the world, and an estimated 5-10 million persons infected with the human immunodeficiency virus (HIV) were at risk of developing AIDS. 50% of AIDS victims have died. It has been reported that after 1 year of clinical use HIV could develop resistance to AZT (azidothymidine), the only effective drug used worlwide and recommended for clinical use by the US government. AIDS has also been treated by acupuncture and moxibustion which recent experiments have associated with improving immune function and enhancing resistance to disease. The American scientists Smith and Naomi Rabinowitz used acupuncture and moxibustion in the clinical treatment of AIDS from 1982 to 1988 when they treated 350 patients with AIDS and AIDS related complex. 1 advanced case with Kaposi's sarcoma and signs of hemorrhage was significantly improved after treatment. Traditional Chinese medicine (TCM) has been used successfully in treating cholera, syphilis, epidemic encephalitis, influenza, and hepatitis with a great variety of clinical treatment measures and experiences. In recent years the treatment of AIDS by TCM using herbs and their extracts has been increasing. Dr. Yu of Santa Barbara, California, Hospital, in cooperation with Dr. Chen of China, successfully treated on AIDS patient with Chinese herbal medicine. The patient was still living and well more than 2 years later when another 24 cases which were not treated with TCM died during the same period. In China there are no special laboratories dealing with the prevention and treatment of AIDS, although scientific HIV research could benefit from such activities. On the other hand, foreign scientists and Chinese abroad have accomplished a significant amount of relevant research.
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PMID:Recent development of studies on traditional Chinese medicine in prophylaxis and treatment of AIDS. 159 94

In human immunodeficiency virus-1 (HIV-1)-infected cell cultures, cell-to-cell fusion and the formation of multinucleated giant cells (syncytia) are induced as a consequence of interactions between the viral envelope glycoprotein on infected cells and cell surface CD4 molecules on uninfected cells. Although activated CD4+ T cells rapidly form syncytia when cultured with HIV-1 envelope glycoprotein expressing (env+) cells, freshly isolated, unstimulated CD4+ T cells do so more slowly. In these studies, we sought to explore the role of T cell activation in rendering CD4+ T cells susceptible to HIV-1-mediated syncytia formation. Our results indicate that within 2 h of exposure to immunologic stimuli, CD4+ T cells acquire the ability to form syncytia with HIV-1 env+ cells. Both cholera toxin, an inhibitor of protein kinase C (PKC) through its effects on inositol triphosphate and diacylglycerol production, and 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride, a noncompetitive inhibitor (with respect to ATP) of PKC, prevented unstimulated but not previously stimulated CD4+ T cells from forming syncytia with HIV-1 env+ cells. 1-Oleoyl-2-acetyl glycerol, an analog of the PKC activator, diacylglycerol, enhanced syncytia formation whereas ionomycin, a calcium ionophore, had no effect. These results suggest that activation of PKC is essential for previously unstimulated CD4+ T cells to become fusogenic.
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PMID:Early activation events render T cells susceptible to HIV-1-induced syncytia formation. Role of protein kinase C. 182 86

With the exception of a few consistent pathogens--Pasteurella multocida strains of bovine hemorrhagic septicemia and fowl cholera, Actinobacillus (Haemophilus) pleuropneumoniae, Haemophilus aegyptius and Haemophilus paragallinarum--members of the family Pasteurellaceae are commensal parasites on mucous membranes of vertebrate animals. Many have pathogenic potential, which becomes manifest under conditions of immunodeficiency and stress. Pathogenesis (except in porcine atrophic rhinitis) depends on mobilization of inflammatory responses probably in large part by endotoxin with contributions from protein toxins, which interfere with leukocyte activity and, by their cytotoxicity, cause exacerbation of the inflammatory reaction. Disease patterns include pneumonic/septicemic, upper respiratory and local/traumatic. Acquired resistance is chiefly antibody-dependent, and, with current and emerging biotechnical resources, stands a good chance of being artificially achievable for many important diseases attributed to Pasteurellaceae.
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PMID:Our understanding of the Pasteurellaceae. 219 10

The etiology, pathogenesis, transmission and communicability, diagnosis, and management of infectious diarrhea are reviewed. Infectious diarrhea is common in both industrialized and unindustrialized areas of the world. Better understanding of the etiology and pathogenesis and identification of "new" enteric pathogens has resulted in the use of a variety of drugs to relieve symptoms or to effect a clinical cure. Both host and microbial virulence factors are key in the acquisition of diarrheal illness. Host factors such as extreme age, a dysfunctional gastrointestinal tract, or underlying immunodeficiency enhance the risk of illness after ingestion of a pathogen or its toxins. Microbial virulence factors (the pathogen's ability to invade or produce enterotoxins, neurotoxins, or cytotoxins) characterize the type of illness manifested and the symptom complex (e.g., acute watery diarrhea versus chronic dysentery). Supportive care is indicated in the majority of cases of infectious enteritis, and rehydration is considered the mainstay of therapy in any diarrheal illness accompanied by dehydration. Antimicrobial therapy is beneficial in the treatment of severe diarrhea caused by Shigella, Campylobacter spp., Vibrio cholerae, Escherichia coli, and Clostridium difficile. Infectious diarrhea is common but is often self-limited and of short duration. Therapy frequently consists of symptomatic relief and fluid replacement.
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PMID:Management and prevention of bacterial diarrhea. 281 19

Vaginal immunization with the Simian immunodeficiency virus (SIV) was investigated in macaques in order to study genital mucosal antibodies. A combined route of genital- and gut-associated lymphoid tissues was used to stimulate IgA and IgG antibodies in vaginal fluid, serum and saliva. Macaques were immunized with a recombinant, particulate SIV antigen (SIV gag P27), covalently linked to the mucosal adjuvant cholera toxin B subunit (CTB). The animals were immunized sequentially as follows: vaginal (x2) followed by oral (x3), or the reverse sequence of immunization. The results show that both vaginal followed by oral immunization or the reverse sequence induces specific p27 IgA and IgG antibodies in the vaginal fluid and serum. IgA antibodies were also detected in saliva. Vaginal IgA antibodies have the secretory component and J chain suggesting that they are of secretory origin.
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PMID:Induction of IgA and IgG antibodies in vaginal fluid, serum and saliva following immunization of genital and gut associated lymphoid tissue. 750 58

The protein E-specific lysis mechanism of the Escherichia coli-specific bacteriophage PhiX174 was employed to produce Vibrio cholerae ghosts (VCG). VCG consist of both rounded and collapsed cells that have lost their cytoplasmic contents through an E-specific hole in the cell envelope. These ghosts are proposed as non-living material for immunization against cholera. A specific membrane anchor sequence was used to insert the human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT) fusion protein into the cell envelope of V. cholerae. The identity of the expression products was confirmed by Western blot analysis employing an RT-specific monoclonal antibody. HIV-1 RT was chosen as a model for the purpose of evaluating heterologous gene expression in V. cholerae and the carrier potential of VCG. Intraperitoneal immunization of mice was used to evaluate the immunogenic potential of VCG. Preliminary results showed significant seroconversions to intact whole-cell vibrio antigens in mice immunized with VCG or a heat-killed whole-cell vibrio preparation.
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PMID:Production of Vibrio cholerae ghosts (VCG) by expression of a cloned phage lysis gene: potential for vaccine development. 753 Aug 88

Control of pandemic infection of human immunodeficiency virus type 1 (HIV-1) requires some means of developing mucosal immunity against HIV-1 because sexual transmission of the virus occurs mainly through the mucosal tissues. However, there is no evidence as yet that the secretory immunoglobulin A (IgA) antibody induced by immunization with antigens in experimental animals can neutralize HIV-1. We demonstrate here that oral immunization with a new macromolecular peptide antigen and cholera toxin (CT) induces a high titre (1:2") of gut-associated and secretory IgA antibody to HIV-1. Using three different neutralizing assays, we clearly demonstrate that this secretory IgA antibody is able to neutralize HIV-1IIIB, HIV-1SF2 and HIV-1MN. Our new approach may prove to be important in the development of a mucosal vaccine that will provide protection of mucosal surfaces against HIV-1.
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PMID:Neutralization of HIV-1 by secretory IgA induced by oral immunization with a new macromolecular multicomponent peptide vaccine candidate. 758 51

Proliferation of normal T lymphocytes is impaired by human immunodeficiency virus (HIV) proteins. In this paper, we demonstrate important parts of this mechanism. Initially, HIV-induced impairment of proliferation was shown to be an active process involving induction of protein tyrosine kinases in both CD4 and CD8 T cells. Furthermore, the impairment of cell proliferation was demonstrated to be linked to induction of the inhibitory protein kinase A (PKA) pathway by HIV proteins. This induction of PKA was accompanied by an increase in intracellular cAMP, which is necessary for the activation of PKA. Finally, increases in cAMP/PKA activity were shown to induce biochemical changes that impaired proliferation when cells were stimulated with phytohemagglutinin. This was demonstrated by showing that (i) agents, other than HIV proteins, that increase cAMP/PKA activity (cholera toxoid and 8-bromo-cAMP) also decreased T-lymphocyte proliferation; (ii) exposure of lymphocytes to HIV or cholera toxoid led to decreased membrane activity of the proliferation promoter protein kinase C upon stimulation; and (iii) agents that reduced cAMP generation neutralized the effect of HIV proteins and restored lymphocyte proliferation. These studies show that the HIV-induced augmentation of cAMP/PKA activity may be a key part of the mechanism responsible for all or part of the HIV-induced anergy of T lymphocytes.
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PMID:Human immunodeficiency virus proteins induce the inhibitory cAMP/protein kinase A pathway in normal lymphocytes. 768 26


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