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)

Macrophages, unlike CD4+ T cells, can be productively infected by human immunodeficiency virus (HIV) without prior cellular activation. Cytopathic infection ensues without the induction of tumor necrosis factor alpha (TNF alpha), interleukin 1 beta (IL-1 beta), interleukin 6 (IL-6), or tissue factor genes. In detailed studies on TNF alpha, HIV infection did not affect the regulation of TNF alpha in response to bacterial lipopolysaccharide. In an effort to examine the interferon responsiveness of HIV-infected macrophages, the cells were challenged with vesicular stomatitis virus (VSV) with or without interferon pretreatment. Surprisingly, HIV-infected macrophages were completely resistant to VSV-induced lysis even in the absence of interferon; however, no interferon was detected in the supernatants of these infected cells. The resistance of HIV-infected macrophages to superinfection with VSV indicates a previously undescribed effect of HIV upon macrophage cellular metabolism.
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PMID:Characterization of a macrophage-tropic HIV strain that does not alter macrophage cytokine production yet protects macrophages from superinfection by vesicular stomatitis virus. 217 98

We constructed a recombinant human immunodeficiency virus (HIV) vector to facilitate studies of virus infectivity. A drug resistance gene was inserted into a gp160- HIV proviral genome such that it could be packaged into HIV virions. The HIV genome was rendered replication defective by deletion of sequences encoding gp160 and insertion of a gpt gene with a simian virus 40 promoter at the deletion site. Cotransfection of the envelope-deficient genome with a gp160 expression vector resulted in packaging of the defective HIV-gpt genome into infectious virions. The drug resistance gene was transmitted and expressed upon infection of susceptible cells, enabling their selection in mycophenolic acid. This system provides a quantitative measure of HIV infection, since each successful infection event leads to the growth of a drug-resistant colony. The HIV-gpt virus produced was tropic for CD4+ human cells and was blocked by soluble CD4. In the absence of gp160, noninfectious HIV particles were efficiently produced by cells transfected with the HIV-gpt genome. These particles packaged HIV genomic RNA and migrated to the same density as gp160-containing virions in a sucrose gradient. This demonstrates that HIV virion formation is not dependent on the presence of a viral envelope glycoprotein. Expression of a murine leukemia virus amphotropic envelope gene in cells transfected with HIV-gpt resulted in the production of virus capable of infecting both human and murine cells. These results indicate that HIV can incorporate envelope glycoproteins other than gp160 onto particles and that this can lead to altered host range. Like HIV type 1 and vesicular stomatitis virus(HIV) pseudotypes, gp-160+ HIV-gpt did not infect murine NIH 3T3 cells that bear human CD4, confirming that these cells are blocked at an early stage of HIV infection.
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PMID:Construction and use of a human immunodeficiency virus vector for analysis of virus infectivity. 221 18

Bloom's syndrome (BS) is an autosomal recessive disease characterized by short stature, sensitivity to sunlight, and telangiectasic malar erythema. It is associated to chromosomal breakage, to primary combined immunodeficiency, and to a high incidence of neoplasias. The authors report the case of two siblings with BS and associated immunodeficiency. Both patients were male and 5 (A) and 4 (B) years old at the time of diagnosis. Chronic diarrhea, recurrent otitis media, purulent rhinitis, conjunctivitis and pyodermatitis were reported by patient A. Patient B was admitted with diagnosis of bilateral neuroblastoma and had the tumor resected. Later on, he presented with oral moniliasis, herpetic stomatitis, and skin abscesses. This patient did not have recurrent infections. Immunological evaluation showed normal serum levels of CH50, C3, and C4 for both patients. Serum IgG, IgA, IgM, and salivary IgA levels were: 455 mg/dl, 15mg/dl, 20mg/dl, 0.6mg/dl for A, and 400mg/dl, 15mg/dl, 20mg/dl, and 0.2mg/dl for B, respectively. Serum antipolio antibodies (1, 2, and 3) were normal, and low levels of isohemagglutinins were observed in both patients. T cells subset determination showed: patient A--OKT3 = 66%, OKT4 = 33%, OKT8 = 32%, and 4/8 ratio = 1.0; patient B--OKT3 = 70%, OKT4 = 32%, OKT8 = 34%, and 4/8 ratio = 1.0. In vitro cellular immune response to PHA was depressed only in patient B. Patients karyotype showed chromosomal breaks with sister chromatid exchanges. Neither patient had abnormal alphafetoprotein and carcinoembryonic antigen serum levels. The rarity of such associations justifies the presentation of the cases.
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PMID:[Familial Bloom's syndrome associated with neuroblastoma]. 221 4

This report describes a case of HIV-associated periodontitis complicated by necrotizing stomatitis in a homosexual male patient with AIDS. Necrotizing stomatitis is a rapidly progressive ulcerative and necrotic infection that causes massive destruction of the oral tissues and underlying bone. Like HIV periodontitis, it appears to be related to the immune suppression caused by human immunodeficiency virus (HIV) infection; importantly, it may be life threatening. In this case, initial resolution resulted from local debridement in association with metronidazole therapy. Long-term clinical management consisted of monthly professional prophylaxis, good oral hygiene, and daily rinses with chlorhexidine. This case suggests that progressive oral necrotizing infection should be recognized as one element in the spectrum of oral manifestations of HIV infection.
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PMID:HIV-associated periodontitis complicated by necrotizing stomatitis. 231 60

The treatment of plasma with organic solvent/detergent mixtures at the time of plasma collection or pooling could reduce the exposure of technical staff to infectious viruses and enhance the viral safety of the final product. Treatment of plasma for 4 hours with 2-percent tri(n-butyl)phosphate (TNBP) at 37 degrees C, with 1-percent TNBP and 1-percent polyoxyethylensorbitan monooleate (Tween 80) at 30 degrees C, or with 1-percent TNBP and 1-percent polyoxyethylene ethers, (Triton X-45) at 30 degrees C resulted in the rapid and complete inactivation of greater than or equal to 10(4) tissue culture-infectious doses (TCID50) of vesicular stomatitis and Sindbis viruses, which are used as surrogates. Treatment of plasma with TNBP and TNBP and Tween-80 was shown to inactivate greater than or equal to 10(4) TCID50 of human immunodeficiency virus. TNBP treatment of plasma contaminated with 10(6) chimpanzee-infectious doses (CID50) of hepatitis B virus and 10(5) CID50 of non-A,non-B hepatitis virus prevented the transmission of hepatitis to chimpanzees. Immediately after treatment of plasma with 2-percent TNBP, the recovery of factors VIII, IX, and V and antithrombin III was 80, 90, 40, and 100 percent, respectively. Recovery of all factors was greater than or equal to 90 percent after treatment with TNBP and detergent mixtures. Treated plasma was fractionated by standard techniques into antihemophilic factor and prothrombin complex concentrates, immune globulin, and albumin. Prior treatment with TNBP or TNBP and detergent did not affect the separations of desired proteins. Therefore, it appears possible to inactivate viruses in plasma before the execution of standard fractionation procedures.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The use of tri(n-butyl)phosphate detergent mixtures to inactivate hepatitis viruses and human immunodeficiency virus in plasma and plasma's subsequent fractionation. 175 94

A murine model of virally induced acquired immunodeficiency was analyzed in mice. The effect of systemic infection with various isolates of lymphocytic choriomeningitis virus (LCMV) on the capacity of mice to mount a T cell-independent IgM and a T cell-dependent IgG neutralizing antibody response against a subsequent infection with vesicular stomatitis virus (VSV) was analyzed. DBA/2 mice infected with the LCMV-WE isolate were impaired in their IgM and IgG responses to VSV. Immune suppression was not caused by interferons inhibiting proper VSV antigen expression, since responses to inactivated VSV were also suppressed. The higher the dose of the LCMV and the lower the dose of the challenging VSV infection the more drastic was the apparent lack of immune responsiveness and the longer it lasted. Kinetics of induction of suppression of the T cell-independent IgM responses closely followed that of a normal cytotoxic T cell response to LCMV-WE, starting on day 6 and reaching maximal levels by day 8 to 10. The T cell-dependent IgG response to VSV was suppressed with a kinetics that was shifted by about 6 days when compared with suppression of IgM responses, i.e. LCMV infection on the same day or before (but not after) VSV infection led to suppression of IgG responses that are usually first detected by day 6-7 after initiation of the VSV infection. Severity and duration of immunosuppressiveness depended upon the LCMV isolate and the mouse strain used: LCMV-WE and LCMV-Docile were most, whereas LCMV-Armstrong was in general least immunosuppressive. Antibody responses to VSV-NJ seemed to be more subject to LCMV-induced immune suppression than VSV-IND-specific responses. Mouse strains differed considerably with respect to extent of suppression, dependent upon both major histocompatibility genes (MHC) and non-MHC genes. DBA and Swiss type mice were generally more susceptible than C57BL and CBA mice, and H-2q and H-2k seemed to be more susceptible than H-2b or H-2d mice. Mice infected with LCMV-WE showed signs of acquired immunodeficiency diseases since they were more susceptible to superinfection with VSV and developed paralytic disease and tended to die from VSV infection. Since LCMV is basically a noncytopathic virus, this murine model of virally induced immune suppression may serve to analyze immune pathogenesis of virus-induced acquired immunodeficiency.
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PMID:An acquired immune suppression in mice caused by infection with lymphocytic choriomeningitis virus. 245 42

The major envelope glycoprotein, gp120, of human immunodeficiency virus type 1 (HIV-1) was purified from a Chinese hamster ovary cell line transfected with a truncated form of the HIV-1 env gene. The recombinant glycoprotein (rgp120) was formulated with aluminum hydroxide adjuvant and was used to immunize chimpanzees. The recombinant preparation was effective in eliciting cellular and humoral immunity as well as immunologic memory. Anti-rgp 120 antibodies reacted with authentic viral gp120 in immunological blot assays and were able to neutralize HIV-1 infectivity in vitro. Sera from the rgp120-immunized animals were able to neutralize HIV-1 pseudotypes of vesicular stomatitis virus prepared from the IIIB isolate, from which the gene encoding rgp120 was derived, as well as two heterologous isolates, ARV-2 and RF. The immune response elicited against the rgp120 was not effective in preventing viral infection after intravenous challenge with HIV-1. The implications of these results on HIV-1 vaccine development are discussed.
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PMID:Human immunodeficiency virus type 1 challenge of chimpanzees immunized with recombinant envelope glycoprotein gp120. 245 98

Dextran sulfate (DS) is a potent inhibitor of the growth of human immunodeficiency virus type 1 (HIV-1) in the H9 cell. Its minimal inhibitory concentration is about 1 microgram/ml. Its therapeutic index is greater than or equal to 200 which is higher than that of 38 for zidovudine. At the ID100 range, DS blocks the synthesis of HIV-1 antigens completely for at least 21 days; zidovudine at the subtoxic concentration of 3 micrograms/ml is incapable of achieving such a complete blockage. DS is still active when added to H9 cell cultures 4 hr after the addition of HIV-1. DS does not inactivate extracellular HIV-1 and is incapable of inducing interferons. It interferes partially with the infection of the H9 cells by the HIV-1. It inhibits the activity of HIV-1 reverse transcriptase. These activities may account, at least in part, for the inhibitory activity of dextran sulfate against the HIV-1. DS has a narrow antiviral spectrum; it is noninhibitory to the herpes simplex, vesicular stomatitis, polio, or adeno viruses. Dextran is not inhibitory to HIV-1. After sulfonation, the sulfonated dextran is highly inhibitory. Therefore, the sulfate group in the DS molecule appears to be essential for its anti-HIV-1 activity. The molecular weights of DS within the range 4000 to 12,000 do not appear to influence its anti-HIV potency.
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PMID:Dextran sulfate as an inhibitor against the human immunodeficiency virus. 246 37

Human immunodeficiency virus (HIV) infection was studied by means of CD4-expressing human-murine T-cell hybrids, containing a variable amount of human chromosomes. Fusion of the HPRT- murine cell line BW5147 with human T-cell acute lymphoblastic leukemia or normal human blood cells resulted in a panel of human-murine T-cell hybrids. For this study, we used four hybrids containing all or several human chromosomes, which all expressed the CD4 antigen, as assessed by different anti-CD4 monoclonal antibodies (e.g., OKT4A, Leu-3a, and MT151) and, in addition, a variable number of other human T-cell antigens. For infection, HTLV-IIIB-infected H9 cells, pretreated with mitomycin C, and cell-free concentrated supernatants from these cells were used. In cells of inoculated cultures of the CD4+ T-cell hybrids, no viral antigen could be demonstrated. Culture supernatants of inoculated hybrids, except for an initial rise due to the virus inoculum, never showed reverse transcriptase activity above background. Cocultivation of these cell cultures with H9 cells did not result in detectable virus replication. Cocultivation of CD4-expressing hybrid cells with HIV-infected cells did not result in syncytium formation. Moreover, these hybrids were resistent to infection with vesicular stomatitis virus (VSV)-HIV pseudotypes. These findings imply that expression of the CD4 antigen on the cell surface is not sufficient for productive infection with HIV. The infectivity block observed in these hybrids seems to occur at the level of virus penetration, presumably at the stage of membrane fusion events.
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PMID:Human immunodeficiency virus infection studied in CD4-expressing human-murine T-cell hybrids. 246 72

Several sulfated polysaccharides (dextran sulfate, pentosan polysulfate, fucoidan, and carrageenans) proved to be potent inhibitors for herpes simplex virus, human cytomegalovirus, vesicular stomatitis virus, Sindbis virus, and human immunodeficiency virus. They were moderately inhibitory to vaccinia virus but not inhibitory to adenovirus, coxsackievirus, poliovirus, parainfluenza virus, and reovirus. These results indicate that, with the exception of parainfluenza virus, enveloped viruses are specifically susceptible to the inhibitory activity of sulfated polysaccharides.
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PMID:Sulfated polysaccharides are potent and selective inhibitors of various enveloped viruses, including herpes simplex virus, cytomegalovirus, vesicular stomatitis virus, and human immunodeficiency virus. 247 75


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