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 homosexual man with AIDS developed multifocal KS with involvement of the palate, larynx, trachea, and esophagus. Symptoms included dysphagia and gagging with resultant inanition. Short-course local radiation therapy effectively resolved the mucosal KS lesions in the treated areas. Other otolaryngologic manifestations included herpes stomatitis and oral candidiasis.
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PMID:Pharyngeal obstruction by Kaposi's sarcoma in a homosexual male with acquired immune deficiency syndrome. 644 93

The relative in vitro antiviral activities of three related nucleoside carboxamides, ribavirin (1-beta-D-ribofuranosyl-1,2,4-triazole-3-carboxamide), tiazofurin (2-beta-D-ribofuranosylthiazole-4-carboxamide), and selenazole (2-beta-D-ribofuranosylselenazole-4-carboxamide), were studied against selected DNA and RNA viruses. Although the activity of selenazole against different viruses varied, it was significantly more potent than ribavirin and tiazofurin against all tested representatives of the families Paramyxoviridae (parainfluenza virus type 3, mumps virus, measles virus), Reoviridae (reovirus type 3), Poxviridae (vaccinia virus), Herpes-viridae (herpes simplex virus types 1 and 2), Togaviridae (Venezuelan equine encephalomyelitis virus, yellow fever virus, Japanese encephalitis virus), Bunyaviridae (Rift Valley fever virus, sandfly fever virus [strain Sicilian], Korean hemorrhagic fever virus), Arenaviridae (Pichinde virus), Picornaviridae (coxsackieviruses B1 and B4, echovirus type 6, encephalomyocarditis virus), Adenoviridae (adenovirus type 2), and Rhabdoviridae (vesicular stomatitis virus). The antiviral activity of selenazole was also cell line dependent, being greatest in HeLa, Vero-76, and Vero E6 cells. Selenazole was relatively nontoxic for Vero, Vero-76, Vero E6, and HeLa cells at concentrations of up to 1,000 micrograms/ml. The relative plating efficiency at that concentration was over 90%. The effects of selenazole on viral replication were greatest when this agent was present at the time of viral infection. The removal of selenazole from the medium of infected cells did not reverse the antiviral effect against vaccinia virus, but there was a gradual resumption of viral replication in cells infected with parainfluenza type 3 or herpes simplex virus type 1 (strain KOS). However, the antiviral activity of ribavirin against the same viruses was reversible when the drug was removed.
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PMID:Broad-spectrum antiviral activity of 2-beta-D-ribofuranosylselenazole-4-carboxamide, a new antiviral agent. 661 11

(+/-)-3-(4-Amino-1H-pyrrolo[2,3-d]pyrimidin-1-yl)-5-(hydroxymethyl)- 1 alpha,2 alpha,3 beta,5 beta)-1,2-cyclopentanediol (9), the carbocyclic analogue of tubercidin, prepared from (+/-)-3-amino-5-(hydroxymethyl)-(1 alpha,2 alpha,3 beta,5 beta)- 1,2-cyclopentanediol (6), is cytotoxic to cells containing adenosine kinase but not to cells that do not, indicating that its activity depends on phosphorylation. Although inactive against P388 leukemia in mice and against herpes and influenza viruses in vitro, it showed marginal activity against respiratory syncytial, vesicular stomatitis, and rhino viruses in vitro.
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PMID:(+/-)-3-(4-Amino-1H-pyrrolo[2,3-d]pyrimidin-1-yl)-5-(hydroxymethyl)- (1 alpha,2 alpha,3 beta,5 beta)-1,2-cyclopentanediol, the carbocyclic analogue of tubercidin. 670 54

4-methyl-2-amino-pyridine-palladiumchlorid (IV) showed an inactivation of cell-free enveloped DNA and RNA viruses in serum-free saline such as vaccinia, pseudorabies, herpes type 1, Newcastle disease and influenza virus A/fowl plague, human influenza type A and B and vesicular stomatitis viruses, and adenovirus, a naked DNA virus, too. Picorna viruses were not inactivated, the inactivation of other viruses failed in medium with 10% serum. However the replication of enveloped viruses as checked with vaccinia and fowl plague viruses was inhibited, also when the compound was present only for 1 h after infection. Contrary to this the multiplication of adenovirus was depressed only with 90%. For the inactivation of viruses high concentrations were necessary than for the inhibition of replication. Therefore more than one kind of mode of action have to be taken into consideration.
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PMID:[On the biological action of transition metal complexes. 2. The antiviral activity of 4-methyl-2-amino-pyridine-palladium-chloride (IV)]. 679 48

A case of severe generalised herpes simplex type 2 infection is described in an adult male who had known exposure to herpes. The patient first complained of headache, fever and neurological symptoms, and three to six days later of conjunctivitis, severe pharyngitis, arthralgia and vesicular lesions about the body. During the first 14 days of illness, including three in hospital, the patient was diagnosed as having infection with varicella virus, vesicular stomatitis virus, or hand-foot-and-mouth disease virus. The diagnosis of infection with herpesvirus was not considered until herpesvirus was visualised in vesicular fluid by electron microscopy six weeks after onset. HSV-2 was then repeatedly isolated from vesicular fluids over the next four years. Detailed serological tests on the patient's sequential serum samples demonstrated a specific and continued response to HSV-2. He possibly acquired the virus iatrogenically, either by oral droplet transmission into or finger contamination of a PPD injection site, from the nurse who administered the injection and then palpated the site.
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PMID:Herpes type 2 infection with unusual generalised manifestations and delayed diagnosis in an adult male. 687 92

A comparative study of various factors of humoral immunity in human chronic herpes stomatitis (CHS) in periods of relapses and remission of the infection showed the exacerbations of the disease to occur in the presence of complement-fixing (CF) and virus-neutralizing (VN) antibodies in the blood serum the titres of which moderately rose with the progress of the infection. A relapse of the disease occurs during marked decline in the content of secretory IgA and true secretory Sc-IgA, serum and secretory IgG, low levels of serum interferon, and a small rise in titres of 19S specific CF antibodies. Remission comes as these values become normal. Although specific immunological changes do occur in CHS, they are not very marked, whereas the factors of nonspecific host resistance change considerably in close correlation with the periods of relapse and remission of the infection.
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PMID:[Humoral immunity factors in the pathogenesis of recurrence in chronic herpetic infection]. 712 14

Comparative studies of various factors of cellular immunity in human chronic herpetic stomatitis (CHS) in periods of relapses and remission of the infection revealed no significant changes in specific cellular immune response, blasttransformation of lymphocytes to herpes simplex virus antigen. At the same time, the indices of nonspecific cellular responsiveness: the rosette-forming activity of T-lymphocytes and the level of leukocyte interferon were markedly reduced in the period of recurrence of the infection and increased as remission developed. The role of immune factors in the pathogenesis of herpes relapses is discussed.
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PMID:[Cellular immunity factors in the pathogenesis of recurrences of chronic herpetic infection]. 713 30

Samples were examined by polymerase chain reaction (PCR) for the presence of the putative Kaposi's sarcoma herpes virus (KSHV). KS DNA from HIV-negative, African, endemic (EKS) samples, and epidemic HIV-positive KS (AKS), and sporadic KS (SKS) samples were tested from Tanzania and Sweden. All of the HIV KS (18 African EKS and 4 Swedish SKS) as well as the HIV-positive AIDS-related KS (16 African and 7 Swedish AKS) biopsies were shown to contain the previously described DNA sequences. KS lesions from children, females, and males in various tissues were analyzed including skin, lymph nodes, gut and oral mucosa. All forms of KS showed a single PCR product of the expected size (233 base pairs). To exclude amplification of other types of herpes virus, virus preparations of Epstein-Barr virus (EBV), herpes simplex virus, cytomegalovirus, vesicular stomatitis, and human herpes virus type 6 (HHV6) were assayed, again by PCR, using the KSHV primers. No PCR products were obtained with any of these virus strains. However, most HIV-positive and HIV-negative KS DNA samples also contained either EBV and/or HHV6 sequences. All biopsies from non-KS tissues (cells) of HIV-positive and HIV-negative individuals were consistently negative for KSHV by PCR. The observation that the same herpes virus-like DNA sequence is present in endemic and sporadic, as well as AIDS-related, Kaposi's sarcoma cases suggests a possible pathogenic association between this putative novel, herpes-like virus and KS. The herpes virus-like DNA sequences described by Y. Chang in 1994 may indeed represent a novel herpes (KSHV), etiopathologically associated with various clinical forms of Kaposi's sarcoma. Its pathogenic importance is indicated by its presence in different KS tissues with various clinical types of KS and its absence from non-KS-involved tissues. Furthermore, the presence of KSHV in KS of children suggests a nonsexual mode of transmission.
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PMID:A role for a new herpes virus (KSHV) in different forms of Kaposi's sarcoma. 758 56

Semliki Forest virus (SFV) enters cells by receptor-mediated endocytosis, followed by acidification of endosomes by the action of the vacuolar H(+)-ATPase. Fusion of the viral and the endosomal membrane delivers the viral genome to the cytoplasm. Direct blockade of the vacuolar H(+)-ATPase by the selective inhibitor bafilomycin A1 (BFLA1) prevented the infection of cells by SFV, if the compound was present during the first minutes of infection. Attachment and penetration of virus particles were not the targets of the antibiotic. BFLA1 and the ionophore monensin potently blocked SFV infection even at low pH, indicating that acidic pH is not sufficient for SFV to deliver its genome to the cytoplasm, but the proper functioning of the H(+)-ATPase pump is necessary. Other enveloped RNA-containing viruses, such as vesicular stomatitis virus or influenza virus were also blocked by BFLA1, whereas no effect was observed with Sendai virus, which enters into cells by direct fusion with the plasma membrane. Enveloped DNA-containing viruses, such as herpes-viruses and vaccinia virus, infected the cells even when the vacuolar H(+)-ATPase was inhibited by BFLA1; similar behaviour was observed with poliovirus and adenovirus. Animal virus particles promote the internalization of proteins and other macromolecules during entry. BFLA1 blocked co-entry of the toxin alpha-sarcin when induced by SFV, but not when induced by Sendai virus. The inhibition of the enzyme responsible for acidification of endosomes by means of the potent inhibitor BFLA1 constitutes a selective and powerful tool to analyse the low-pH dependent mechanism(s) during virus entry and will aid in understanding the mechanisms and routes of entry of animal viruses into cells.
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PMID:Involvement of the vacuolar H(+)-ATPase in animal virus entry. 793 Nov 46

Oral mucosal inflammation evolves in response to microbial pathogens and non-infectious antigens which activate humoral and cell-mediated immunologic processes. Most of these disease processes invoke a leukocyte response culminating in cellular infiltration of the submucosa and, to some degree, transmigration into the epithelium itself. Calprotectin, a leukocyte-derived dimeric protein complex that has potent antibacterial and antifungal effects, has recently been identified in skin and mucosal keratinocytes implying that epithelium may biochemically contribute to the overall mechanism of host defense. In this study, the upregulation of calprotectin as assessed immunohistochemically is pursued for oral diseases of immunopathologic, fungal and viral origin. In lichen planus, candidiasis, herpes virus stomatitis, and oral hairy leukoplakia, calprotectin was found to be expressed to a significantly higher level than in normal control mucosal samples.
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PMID:Keratinocyte expression of calprotectin in oral inflammatory mucosal diseases. 822 66


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