Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0038362 (stomatitis)
8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A new retrovirus was recently discovered in cats affected with an immunodeficiency syndrome (AIDS). The virus shows morphological and biological similarities with the human immunodeficiency virus (HIV), which causes AIDS in human individuals. As the T-lymphocyte is the primary target of the virus, it is termed Feline T-Lymphotropic Lentivirus (FTLV). FTLV is not antigenically related to HIV. Transmission of the virus from animals to human subjects has not been recorded. Cats infected with this virus showed lymphadenopathy, leukopenia, anorexia, chronic stomatitis/gingivitis and other opportunistic forms of infection. Neurological symptoms were also observed. Research is focused on diagnosis, treatment and prevention. Results obtained may contribute to research on AIDS in human subjects.
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PMID:[Infections with feline T-lymphotropic lentivirus]. 284

The human promyelocytic leukemia cell line HL-60 overexpresses the c-myc protooncogene. A calculated secondary structure for c-myc mRNA placed the initiation codon in a bulge of a weakly base-paired region. Treatment of HL-60 cells with 5' d(AACGTTGAGGGGCAT) 3', complementary to the initiation codon and the next four codons of c-myc mRNA, inhibited c-myc protein expression in a dose-dependent manner. However, treatment of HL-60 cells with 5' d(TTGGGATAACACTTA) 3', complementary to nucleotides 17-31 of vesicular stomatitis virus matrix protein mRNA, displayed no such effects. These results agree with analogous studies of normal human T lymphocytes [Heikkila, R., Schwab, G., Wickstrom, E., Loke, S. L., Pluznik, D. H., Watt, R. & Neckers, L. M. (1987) Nature (London) 328, 445-449], except that only one-third as much oligomer was needed for a comparable effect. Proliferation of HL-60 cells in culture was inhibited in a sequence-specific, dose-dependent manner by the c-myc-complementary oligomer, but neither the oligomer complementary to vesicular stomatitis virus matrix protein mRNA nor 5' d(CATTTCTTGCTCTCC) 3', complementary to nucleotides 5399-5413 of human immunodeficiency virus tat gene mRNA, inhibited proliferation. It thus appears that antisense oligodeoxynucleotides added to myc-transformed cells via culture medium are capable of eliciting sequence-specific, dose-dependent inhibition of c-myc protein expression and cell proliferation.
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PMID:Human promyelocytic leukemia HL-60 cell proliferation and c-myc protein expression are inhibited by an antisense pentadecadeoxynucleotide targeted against c-myc mRNA. 327 86

This is a report of a 24-year follow-up of a man now 33 years of age, who suffers almost continuously from severe inflammatory lesions of the lips, nose and eyelids, with increased susceptibility to respiratory infections since early childhood. The condition, previously described as "pyo-rhino-blepharo-stomatitis vegetans (McCarthy)", was treated with systemic corticosteroids and antimicrobial agents for years, but failed to improve until the immune status of the patient was checked after withdrawal of the steroids. T lymphocytes were found to be abnormal as to count in peripheral blood and various functional qualities determined in vivo and in vitro. For treatment, levamisole and thymopoietin pentapeptide (TP-5) were given. Subsequently each drug induced rapid and complete clearing of all lesions, but was followed by the recurrence of facial periorificial lesions after drug withdrawal. Change of the regimen by administering either inosiplex orally or commercial calf thymus extract parenterally, remained ineffective. During therapy with levamisole as well as TP-5, the number of T lymphocytes in peripheral blood normalized, yet impaired functions failed to improve. There was an elevated ratio of T-suppressor/T-inducer cells in blood using OKT antibodies. In vitro testing of different functions of polymorphonuclear leucocytes revealed normal results except for a slight decrease of chemotactic activity during levamisole. In view of the long clinical course, the mass of clinical and immunological data collected over decades, and the therapeutic results as a whole, the disease can be characterized as a peculiar type of pluriorificial pyoderma vegetans, caused by a distinct immunodeficiency of T lymphocytes.
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PMID:[Pyoderma vegetans of facial orifices in T-cell immunodeficiency]. 660 52

Nine foals with combined immunodeficiency were given hepatic and thymus cells from 68- to 110-day-old (gestational age) fetuses or peripheral blood lymphocytes from nonrelated horses. Clinical signs and lesions consistent with graft vs host reaction were observed in eight of the foals. Diarrhea was observed in these 8 foals, and ulcerative dermatitis, stomatitis, or glossitis was detected in 6 of the 8 foals. Histopathologic changes consisting of necrosis and lymphocyte infiltration were observed in liver, skin, alimentary tract, and less frequently in lymphoid tissues. Changes in complete blood counts, plasma bilirubin concentration, and serum sorbitol dehydrogenase activity were compared with sequential histopathologic alterations in the liver of two combined immunodeficiency foals given peripheral blood lymphocytes from unrelated donor horses. Elevations of sorbitol dehydrogenase correlated with the onset and increasing severity of hepatic lesions.
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PMID:Graft versus host reactions in foals with combined immunodeficiency. 698 99

We report here on a 36-year old, HIV-positive patient, who was sent to hospital with an anal fistula. A short time later during the course of an extensive diagnosis the anal fistula was recognized as an extrapulmonary manifestation of a miliary tuberculosis stemming from an immunodeficiency syndrome. A rapid conversion of the sputum, a normalization of the radiological findings and the absence of relapse are the results of the classic systemic fourfold therapy with myambutol, isoniazid, rifampicin and streptomycin. The danger of overlooking the fact that an anal fistula can be the clinically primary manifestation of a tuberculosis and the problems of a mixed infection within the scope of the acquired immunodeficiency syndrome are discussed. Tuberculosis as a frequent complicating infection of HIV-positive patients--often diagnosed some time before the AIDS-infection as in our patient--can be successfully cured by a high dose of intravenous pharmacotherapy, even when additional complications (parasitic stomatitis, increasing deterioration of the immunological parameters) are present. In order to show the large spectrum of the problems involved in the diagnosis, the therapy and the course of the active acquired immunodeficiency syndrome, we have focused here on the detailed description of the case report.
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PMID:[Tuberculous anal fistula in acquired immunologic deficiency syndrome]. 748 36

Cellular mechanisms that control susceptibility to opportunistic infection in human immunodeficiency virus (HIV)-infected individuals remain poorly understood. HIV may induce certain cellular genes that restrict HIV replication and protect cells against other superinfecting viral pathogens. Indeed, HIV-infected monocytes resist infection by vesicular stomatitis virus (VSV). HIV-induced VSV interference in monocytes increases with time after HIV infection. Such interference was evident 6 h after HIV infection and reached maximal levels at 14 days. Monocytotropic but not T cell-tropic HIV strains elicited these effects, signaling a requirement for viral entry and/or replication. Viral interference was independent of interferon (IFN) and was unaffected by addition of neutralizing IFN-alpha and -beta antibodies. The well-described IFN-alpha-inducible antiviral pathways were examined to determine their relationship to the cellular mechanism(s) underlying VSV interference. HIV and IFN-alpha both induced the expression of 2-5A synthetase and Mx gene. In contrast, the guanylate-binding protein (GBP), 6-16, and 9-27 cellular genes were up-regulated by IFN-alpha but not HIV. MxA was detected in HIV-infected monocytes but not in uninfected monocytes. The association between Mx expression and resistance to VSV, coupled with previously described anti-VSV activities by human MxA, suggested that Mx may be an effector molecule for the HIV-induced anti-VSV activities. These results, taken together, suggest that HIV can induce antiviral cellular gene expression, independent of IFN.
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PMID:Regulation of interferon-alpha-inducible cellular genes in human immunodeficiency virus-infected monocytes. 750 41

While considerable progress in examining the course of human immunodeficiency virus (HIV) infection in adults has been made, a better understanding of the natural history of perinatal HIV infection remains to be obtained. Dysregulation of the production and functions of various cytokines, especially the interferons (IFNs), during HIV infections has been reported. Using an in vitro model system, we examined the effects of the HIV type 1 envelope protein, gp120 (10, 50, and 100 ng/ml), on gamma IFN (IFN-gamma) and IFN-alpha production by lymphocytes from neonates and adults and also examined the potential regulatory effects of gp120 on phorbol 12-myristate acetate (PMA)- and Sendai virus-induced IFN-gamma and IFN-alpha production by lymphocytes. PMA at a concentration of 50 ng/ml plus 50 ng of calcium ionophore A23187 per ml was used to induce IFN-gamma, while 150 hemagglutinating units of Sendai virus was used to induce IFN-alpha production. The antiviral activity of both IFN-alpha and IFN-gamma in leukocyte culture supernatants was assayed on BG-9 cells by a dye uptake technique using vesicular stomatitis virus as a challenge virus. Placental cord blood leukocyte (CBL) samples from healthy, term infants and adult peripheral blood leukocytes (APBL) produced no IFN in response to gp120. However, CBL produced significantly decreased levels of IFN-gamma compared with APBL in response to PMA plus ionophore. gp120 significantly suppressed both Sendai virus-induced IFN-alpha and PMA-induced IFN-gamma production by both CBL and APBL in a dose-dependent manner. However, gp120-induced suppression of IFN-alpha and IFN-gamma was significantly greater with CBL than with APBL. Treatment of CBL and APBL with gp120 did not induce any phenotypic alteration of the CD45 RO+ subset. Increased suppression of IFN-alpha and IFN-gamma production by gp120 in neonates may partially explain their apparent increased susceptibility to the clinical progression of HIV infections compared with that of adults.
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PMID:Differential effects of human immunodeficiency virus type 1 envelope protein gp120 on interferon production by mononuclear cells from adults and neonates. 758 19

Human plasma-derived protein concentrates intended for clinical use must be treated for viral inactivation to ensure patient safety. This study explored the use of liquid iodine for inactivation of several lipid- and nonlipid-enveloped viruses in an antithrombin III (AT-III) concentrate. Iodine at levels of 0.01% to 0.02% caused between 43% and 94% loss of AT-III activity, as well as degradation of AT-III as shown by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and Western blot analysis. However, addition of up to 0.1% human albumin protected the AT-III against both inactivation and fragmentation. At albumin levels sufficient to retain greater than 75% of AT-III activity, greater than 6 logs of sindbis, encephalomyocarditis, and vesicular stomatitis viruses, greater than 4 logs of pseudorabies, and greater than 3 logs of human immunodeficiency virus were inactivated. Except with sindbis virus, this represented complete inactivation of all the viruses spiked into the AT-III concentrate.
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PMID:Iodine-mediated inactivation of lipid- and nonlipid-enveloped viruses in human antithrombin III concentrate. 760 9

The mechanism of the antiviral activity of hypericin was characterized and compared with that of rose bengal. Both compounds inactivate enveloped (but not unenveloped) viruses upon illumination by visible light. Human immunodeficiency and vesicular stomatitis viruses were photodynamically inactivated by both dyes at nanomolar concentrations. Photodynamic inactivation of fusion (hemolysis) by vesicular stomatitis, influenza, and Sendai viruses was induced by both dyes under similar conditions (e.g., I50 = 20-50 nM for vesicular stomatitis virus), suggesting that loss of infectivity resulted from inactivation of fusion. Syncytium formation, between cells activated to express human immunodeficiency virus gp120 on their surfaces and CD4+ cells, was inhibited by illumination in the presence of 1 microM hypericin. Hypericin and rose bengal thus exert similar virucidal effects. Both presumably act by the same mechanism--namely, the inactivation of the viral fusion function by singlet oxygen produced upon illumination. The implications of this photodynamic antiviral action for the potential therapeutic usefulness of both hypericin and rose bengal are discussed.
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PMID:Photodynamic inactivation of infectivity of human immunodeficiency virus and other enveloped viruses using hypericin and rose bengal: inhibition of fusion and syncytia formation. 767 35

Besides its role in viral assembly, the vesicular stomatitis virus (VSV) matrix (M) protein causes cytopathic effects such as cell rounding (D. Blondel, G. G. Harmison, and M. Schubert, J. Virol. 64:1716-1725, 1990). DNA cotransfection assays demonstrated that VSV M protein was able to inhibit the transcription of a reporter gene (B. L. Black and D. S. Lyles, J. Virol. 66:4058-4064, 1992). We have confirmed these observations by using cotransfections with an infectious clone of human immunodeficiency virus type 1 (HIV-1) and found that the amino-terminal 32 amino acids of M protein which are essential for viral assembly were not required for this inhibition. For the study of the potential role of M protein in the shutoff of transcription from chromosomal DNA, we have isolated stable HeLa T4 cell lines which encode either a wild-type or a temperature-sensitive (ts) VSV M gene under control of the HIV-1 long terminal repeat promoter. Transcription of the M mRNA was transactivated after HIV-1 infections. A cell line which encodes the wild-type M protein was nonpermissive for either HIV-1 or HIV-2. A cell line that encodes the ts M gene was transfected with the infectious HIV-1 DNA or was infected with HIV-1 or HIV-2. In all cases, at 32 degrees C, the permissive temperature for M protein, the cells were nonpermissive for HIV replication. At 40 degrees C, the ts M protein was nonfunctional and both HIV-1 and HIV-2 were able to replicate at high levels. A comparison of the amounts of proviral HIV-1 DNAs and HIV-1 mRNAs at 10 and 36 h after HIV-1 infection demonstrated that proviral insertion had not been prevented by M protein and that the block in HIV-1 replication was at the level of proviral expression. The severe reduction of HIV-1 proviral transcripts demonstrates that the VSV M protein alone can inhibit expression from chromosomal DNA. These results strongly support the hypothesis that the VSV M protein is involved in the shutoff of host cell transcription. M protein was able to attenuate HIV-1 infections and protect the cell population from HIV-1 pathogenesis. The temperature-dependent switch from a persistent to a lytic HIV-1 infection in the presence of ts M protein could be useful for studies of HIV-1 replication and pathogenesis.
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PMID:Inducible and conditional inhibition of human immunodeficiency virus proviral expression by vesicular stomatitis virus matrix protein. 774


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