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 total of 17 children, aged 1 to 15 years, with gingivostomatitis were investigated to follow the development of immune parameters in those who suffered from herpes simplex virus stomatitis. Mouth swabs were obtained during the acute attack. Blood samples were collected on this occasion and again about 3 weeks later. Humoral immunity to herpes simplex virus was investigated by a complement fixation test and by an antibody-dependent cell-mediated cytotoxicity test. Cell-mediated immunity was investigated in a blast transformation assay with herpes simplex virus type 1 antigen and phytohemagglutinin. Interferon production in herpes-stimulated cultures was measured. Thirteen patients had a herpes simplex stomatitis. Twelve of these children were negative in the complement fixation test on the first serum specimen, but only five were negative in the antibody-dependent cell-mediated cytotoxicity test. These five were still febrile at the time of investigation. Blast transformation was negative at the first investigation in most children, whereas interferon was produced both in leukocyte cultures obtained during the infection and also in cultures made 3 to 4 weeks after the infection. An increase in immune parameters was seen in all patients with herpes stomatitis. From results in blast transformation and antibody-dependent cell-mediated cytotoxicity, it is seen that cell-mediated and humoral immunity can be found at the same time during recovery from this type of infection.
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PMID:Cellular and humoral immune responses to herpes simplex virus during and after primary gingivostomatitis. 73 Mar 66

In accordance with the system of viral species, viral disorders of the oral mucosa may be classified with regard to their intensity of affection. There are but few viral infections exclusively affecting the oral mucosa like e.g. 1. Glossitis papulosa of Michelson, representing a special form of vaccinia inoculata, 2. Gingivo-stomatitis herpetica and 3. warts of the mucosa or condyloma-like papillomas of the oral mucosa including oral papillomatosis, that, itself shows morphological and clinical similarities to laryngeal papilloma. A second group of disorders mainly affecting the oral mucosa includes the "Aphthoid of Pospischill and Feyrter", Zahorsky's herpangina and other viral infections by the Coxsackie group, like vesicular stomatitis. The 3rd group represents viral infections of other organs in which affection of the oral mucosa is a prerogative, e.g. smallpox, varicella, foot-and-mouth disease and pharyngo-conjunctival fever. A 4th group includes those viral infections of the organs in which co-affection of oral mucosa occurs frequently or once in a while (at occasions). Here, we find eczema vaccinatum, herpes zoster, herpes simplex of the oral mucosa mostly on the hard palate, eczema herpeticatum, post-herpetic Erythema exsudativum multiforme, Mononucleosis infectiosa Pfeiffer, viral flu, German measles, parotitis epidemica, rubeola and ECHO-exanthema. A 5th and last group is made up by viral infections of other organs, in which affection of the oral mucosa hardly occurs at all. This group contains paravaccinal Ecthyma contagiosum, poliomyelitis, viral infection of the city of Marburg and some Arbovirus infections. Relatively few viral disorders never co-exist with lesions on the oral mucosa like e.g. Virus-hepatitis or some viral encephalitides. Groups 1 and 2, most important of all, are presented in detail regarding clinics, diagnostics, differential-diagnosis and therapy. The disorders within the other 3 groups are discussed only regarding their importance in the field of ENT-related symptoms of the oral mucosa. A number of pictures and tables completes important clinical details and give further hints to their differential-diagnosis.
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PMID:[Virus diseases of the mouth mucosa]. 83 Jan 6

Most individuals are infected with Herpes Simplex in childhood usually suffering a mild febrile illness of no consequence. Later some individuals suffer recurrent infections which appear as cold sores on the lip while others intermittently shed virus in the oro-pharygeal secretions. Adults uninfected in childhood may be exposed to viruses for example by kissing and develop an acute primary herpes with fever and gingivo-stomatitis occasionally requiring hospital admission. Awareness of this condition is required for diagnosis after which the majority of patients seen in otolaryngological practice need only supportive therapy, explanation and reassurance. Recurrent cold sores are no more that a nuisance in most patients, but occasionally they are severe and in others the cold sore may precipitate oral erythema multiforme. Unfortunately the treatments available for recurrent cold sores are rather unsatisfactory.
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PMID:Oral manifestations of herpes simplex virus infections. 86 5

A miniature pig kidney cell line has been established from porcine fetuses taken aseptically by hysterectomy and maintained for more than 50 passages in Eagle's minimal essential medium containing 10% heat-inactivated newborn calf serum. Cell transfers were performed each week. Primary and serially passaged cells were found to be highly refractory to infection by Chlamydia trachomatis strains TW-3, Bour, and LGV 440L and Chlamydia psittaci strains meningopneumonitis and 6BC and insusceptible to poliovirus type 1. The cells were susceptible to vesicular stomatitis virus and herpes simplex type 1 virus. Identity of the cells was established by cytotoxicity, isozyme, and cytogenetic studies.
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PMID:Characterization of miniature pig kidney cells and their resistance to chlamydial infection. 94 2

In this study, we have analysed the effects of cAMP inducers on the multiplication of vesicular stomatitis virus (VSV) and herpes simplex virus type 1 (HSV-1) in mouse macrophage-like cells. The addition of dibutyryl cAMP (dB-cAMP) or cholera toxin to resting peritoneal macrophages aged in vitro or P388D1 cells resulted in a 10- to 100-fold reduction of VSV yield compared to control cultures. In contrast, no cAMP-dependent inhibition was found in VSV-infected L929 cells. In macrophage-like cells, the dB-cAMP-induced antiviral state was not inhibited by antibodies to interferon (IFN)-alpha/beta and did not correlate with any increase in the intracellular levels of 2-5 oligo(A) synthetase. Dibutyryl cAMP did not inhibit virus yields in mouse macrophages infected with encephalomyocarditis virus. In P388D1 cells, the addition of dB-cAMP resulted in an approximately 10-fold inhibition of HSV-1 replication with respect to control cultures, as evaluated both by TCID50 and plaque assays on Vero cells. Dibutyryl cAMP did not affect VSV binding or entry into mouse macrophages and the cAMP-mediated anti-VSV state was significantly reduced by inhibitors of protein kinase C (i.e. staurosporine and H7). These data suggest that macrophages may acquire resistance to infection by VSV and HSV-1 after treatment with cAMP inducers. This cAMP-mediated antiviral activity does not depend on the modulation of the endogenous IFN system, suggesting that macrophages exhibit multiple resistance mechanisms (i.e. IFN-dependent and IFN-independent) to maintain their intrinsic antiviral activity.
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PMID:Cyclic AMP-mediated inhibition of vesicular stomatitis virus and herpes simplex virus replication in mouse macrophage-like cells. 127 3

Various polyoxometalates proved inhibitory to the replication of a number of enveloped DNA and RNA viruses, i.e., herpesviruses (herpes simplex and cytomegalo), togaviruses (Sindbis), paramyxoviruses (respiratory syncytial), rhabdoviruses (vesicular stomatitis), arenaviruses (Junin and Tacaribe), and retroviruses [human immunodeficiency virus type 1 (HIV-1) and type 2 (HIV-2), simian immunodeficiency virus, and murine sarcoma virus]. The most potent compounds, i.e., JM1590 [K13[Ce(SiW11O39)2]. 26H2O] and JM2766 [K6[BGa(H2O)W11O39]. 15H2O], inhibited HIV-1 and simian immunodeficiency virus at concentrations as low as 0.008-0.8 microM. The polyoxometalates also inhibited giant cell formation in co-cultures of HIV-infected HUT-78 cells and uninfected MOLT-4 cells. Studies designed to unravel the mechanism of action of these compounds revealed that they inhibit the reverse transcriptase activity associated with HIV. The polyoxometalates also proved inhibitory to the binding of HIV-1 virions to the cells. From "time of addition" experiments, whereby the polyoxometalates were added at different times after virus infection, their mechanism of anti-HIV action could be attributed to inhibition of virus-cell binding. There was a good correlation (r = 0.84) between the inhibitory effects of the compounds on HIV-1-induced cytopathicity and their inhibitory effects on syncytium formation and a close correlation (r = 0.902) between their inhibitory effects on syncytium formation and their interaction with gp120, whereas there was no correlation between their anti-HIV-1 activity and their inhibitory effects on HIV-1 reverse transcriptase. In flow cytometric studies, the compounds did not interfere with the binding of OKT4A/Leu-3a monoclonal antibody to the CD4 receptor of uninfected cells, but they inhibited binding of anti-gp120 monoclonal antibody to HIV-1-infected cells. Thus, the binding of the polyoxometalates to the viral envelope glycoprotein gp120 is responsible for their anti-HIV activity.
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PMID:Mechanism of anti-human immunodeficiency virus action of polyoxometalates, a class of broad-spectrum antiviral agents. 128 64

The effect of cicloxolone sodium (CCX) on the replication of vesicular stomatitis virus (VSV) was investigated. The drug was active during all stages of the virus replication cycle, indicating that it does not operate by the specific inhibition of any single essential virus gene product. The drug reduced the number of VSV particles assembled and released by 100- to 1000-fold. Infectious virus yield was reduced 1000- to 10000-fold, giving a 10-fold or greater increase in the particle/p.f.u. ratio. The reduced number of virus particles produced in the presence of CCX results from two superimposed effects: suppression of VSV secondary transcription and viral protein synthesis, and perturbation of virion assembly. The inhibition of VSV assembly is due to impairment of a Golgi apparatus function related to transport of VSV glycoprotein G to the cell surface, and is characterized by accumulation of viral G and M proteins within the cell. Incubation of VSV-infected cells in the presence of two glycosylation inhibitors, tunicamycin and monensin, similarly leads to intracellular accumulation of G and M proteins, suggesting a common mechanism of action affecting VSV virion assembly. The differential effect of CCX concentration on intracellular levels of the L, N and NS proteins was analysed. CCX also possesses a virucidal effect on mature infectious VSV particles in suspension, 300 microM reducing the VSV titre about 10-fold in 24 h at 4 degrees C or 37 degrees C. The mode of antiviral activity against VSV is compared with that against herpes simplex virus.
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PMID:The effect of cicloxolone sodium on the replication of vesicular stomatitis virus in BSC-1 cells. 131 61

The effect of cicloxolone sodium (CCX) on the replication of typical representatives of different virus families [adenovirus type 5 (Ad-5), reovirus type 3 (Reo-3), Bunyamwera and Germiston viruses, poliovirus type 1 (Polio-1) and Semliki Forest virus (SFV)] in tissue culture was investigated. The Golgi apparatus inhibitor monensin (Mon) and CCX were shown to have analogous effects on some aspects of virus replication. Although the Mon-like effect of CCX played no role in the antiviral activity against Ad-5, Reo-3 or Polio-1, it could entirely account for the antiviral activity against the Bunyamwera and Germiston viruses, for which inhibition of glycoprotein processing was responsible for the antiviral activity. In the case of SFV, the Mon-like activity of CCX caused cytoplasmic assembly of fully infectious SFV within vacuoles and thus impaired virus release without altering total infectious virus yield. Fewer Ad-5 and Reo-3 progeny were produced in the presence of the drug. CCX had a dose-dependent biphasic effect on the particle:p.f.u. ratio of the Reo-3 yield. At low CCX concentration (less than 50 microM) the virus yield contained poor quality, non-infectious virus, but at higher CCX concentration (greater than or equal to 100 microM) low quality virus could no longer be successfully assembled. We conclude that the antiviral effect can be manifested in three ways: (i) by a reduction in the virus particle yield produced; (ii) by a loss of quality (relative infectivity); (iii) by a virucidal effect of the drug. We have previously defined three CCX sensitivity classes. Mechanisms (i), (ii) and (iii) operate against viruses belonging to class CCXs-1 [herpes simplex virus (HSV) type 1, HSV-2 and vesicular stomatitis virus], but essentially only (i) and (ii) affect Reo-3 (CCXs-2), whereas (i) and possibly (iii) affect Ad-5 (CCXs-2). In the case of SFV (CCXs-3) none of these mechanisms operate, but relocation of assembled virus is found.
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PMID:The effect of cicloxolone sodium on the replication in cultured cells of adenovirus type 5, reovirus type 3, poliovirus type 1, two bunyaviruses and Semliki Forest virus. 131 62

Prevention and treatment of oral disease is required to maintain quality of life and to improve prognosis of patients infected with the human immunodeficiency virus (HIV). Management requires a team approach, and close collaboration with the appropriate responsible physicians and other health care workers is necessary. Oral infection is frequent and usually opportunistic, and management is based on certain principles. Infections may disseminate and can be persistent and severe; multiple concurrent or consecutive infections with different microorganisms are frequent; fungal, viral, and parasitic infections are rarely curable; and long-term antimicrobial therapy may be required. This article reviews the management of oral candidiasis, hairy leukoplakia, and infections with herpes simplex virus, varicella-zoster virus, and cytomegalovirus. The management of Kaposi's sarcoma, lymphomas, aphthous ulceration, gangrenous stomatitis, bleeding, xerostomia, and adverse drug reactions is also described. Treatment should avoid further immunosuppression and inducement of xerostomia or caries, and should be designed to avoid adverse drug reactions and possible drug interactions.
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PMID:Management of oral health in persons with HIV infection. 131 92

Beginning with 3-cyclopenten-1-ylamine hydrochloride, the 5'-nor derivatives of carbocyclic 2'-deoxyguanosine (2), 2'-deoxyadenosine (3), and 2,6-diaminopurine 2'-deoxyribofuranoside (4) have been prepared. These compounds were evaluated for antiviral potential versus herpes simplex virus, varicella-zoster virus, cytomegalovirus, vaccinia virus, vesicular stomatitis virus, and human immunodeficiency virus and found to lack activity. Also, compounds 2-4 were virtually nontoxic toward the host (human diploid fibroblast ESM and HEL) cells. These biological properties may be due to the inability of 2-4 to be phosphorylated to the requisite nucleotide level that is likely to be necessary for biological activity by correlation to carbocyclic 2'-deoxyguanosine (1), which possesses significant antiviral properties as a result of conversion to its 5'-triphosphate derivative.
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PMID:(+-)-carbocyclic 5'-nor-2'-deoxyguanosine and related purine derivatives: synthesis and antiviral properties. 131 91


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