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)

Human embryonic lung (MRC-5), feline embryo (FEA), mink lung (Mv1Lu) and monkey kidney (BSC-1) cells infected by respiratory syncytial virus showed characteristic morphological changes when viewed by scanning electron microscopy. The surfaces of respiratory syncytial virus-infected cells developed a profusion of slender filaments after 48 h incubation at 31 degrees C. Similar changes in surface morphology were observed in BSC-1 cells infected by murine pneumonia virus. Filament production therefore appears to be a common property of pneumo-viruses. Filaments were not observed in cells infected with either syncytial and non-syncytial herpes simplex virus, the cytocidal vesicular stomatitis and Batai (Bunyaviridae) viruses, or the focus-inducing rabbit fibroma virus. Filament production was not observed in cells infected with ts mutants of respiratory syncytial (RS) virus during incubation at the restrictive temperature, or in a persistently infected culture of BSC-1 cells at 37 degrees C. The persistently infected cells (the RS ts 1/BSC-1 line) had some of the characteristics of cells transformed by oncogenic viruses, namely ability to overlap adjacent cells and agglutination by a low concentration of concanavalin A. The pseudo-transformed phenotype was temperature-dependent, however, and suppressed by raising the temperature of incubation to 39 degrees C. The presence of virus antigen at the cell surface was similarly temperature-dependent in these cells, diminished at high temperature (39 degrees C) and enhanced at low temperature (31 degrees C), suggesting that the changes in the host cell were the result of insertion of virus protein into the cell membrane. Evidently, persistent infection by a cytoplasmic virus can produce alterations in the host cell usually associated with transformation by nuclear viruses.
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PMID:Pneumoviruses: the cell surface of lytically and persistently infected cells. 11 36

Demethylchlortetracycline (DMCT), doxycycline and, to a lesser extent, chlortetracycline were capable of mediating the in vitro photoinactivation of Venezuelan equine encephalitis (VEE) virus. Other tetracyclines tested were found to be inactive in this respect. However, no correlation between chemical structure and photosensitizing activity could be established. The photoinactivation of VEE virus by DMCT proceeds through a photodynamic mechanism as shown by the absolute requirement of O2 for the inactivation to take place. The photoinactivating effect of DMCT was also exerted upon other animal viruses tested, i.e. vesicular stomatitis virus, herpes simplex virus and poliovirus, even when, in the case of poliovirus, the capsid seems to be impermeable to the tetracycline. The fact that the two most effective photosensitizing tetracyclines for VEE virus are also the drugs more frequently associated with drug-induced phototoxicity in humans, suggests that virus photoinactivation could be used as a screening procedure for potentially phototoxic drugs developed for human application.
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PMID:Tetracycline-mediated photodynamic inactivation of animal viruses. 12 Apr 11

Lymphocytes from individuals with laboratory evidence of prior infection with herpes simplex virus (HSV) type 1 or type 2 demonstrated transformation (av antigens. Higher stimulation indexes were obtained when lymphocytes were incubated with the homologous as compared with the heterologous antigen. Higher mean lymphocyte stimulation indexes were also demonstrated in seropositive as compared with seronegative individuals. Lymphocytes from children with HSV-1 stomatitis usually became responsive to HSV-1 antigen within 2 to 6 weeks after the onset of illness. Lymphocytes from infants with neonatal HSV-2 infection were stimulated by HSV-2 antigen.
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PMID:Stimulation of human lymphocytes by Herpes simplex virus antigens. 16 88

Ocular viral infections are a major cause of loss of vision and their effective control by applications of chemical compounds has been extensively investigated. To achieve such a control, better understanding of virus-host-drug interactions become a necessity. Two models, hamster and rabbit cornea, were selected for assays of protection afforded by tilorone dihydrochloride against herpes simplex (HSV) and vesicular stomatitis viruses (VSV). To obtain basic biologic comparison between viral interference and interferon-induction by tilorone, the hamster cornea system was first studied to produce a mutual viral interference by double infection. Furthermore, its effect against ascending herpetic ocular infection into encephalitis was evaluated in the rabbit. This compound was reported to have promising results in improving manifestations such as corneal ulceration, uveitis and conjunctivitis.
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PMID:The mode of inhibition of herpes simplex and vesicular stomatitis ocular viral infections in the rabbit and hamster by an interferon inducer tilorone dihydrochloride. 16 23

Cytopathic changes and virus-specific antigens developed in, then disappeared from, mouse fibroblasts infected by a strain of human cytomegalovirus (CMV), but their disappearance was delayed in cells treated with idoxuridine prior to infection. The replication of vesicular stomatitis virus and herpes simplex virus was restricted in human CMV-infected mouse cells as long as human CMV-specific antigens were present. Virus-specific antigens could be induced by treatment with idoxuridine or arginine deficiency in mouse cells which had previously turned "negative".
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PMID:Virus-specific changes in mouse cells inoculated with a strain of human cytomegalovirus. 16 41

A fraction of mouse RNA containing messenger RNA coding for mouse interferon was translated with high efficiency in a wheat germ system into a fully active product. This product fulfills the criteria for mouse interferon, namely: (1) it was active against vesicular stomatitis virus and herpes simplex virus in mouse cells; (2) its antiviral activity was species specific; (3) its activity was completely neutralized by mouse anti-interferon serum. The synthesis of interferon in this cell-free system requires the presence of spermine.
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PMID:Biosynthesis of mouse interferon by translation of its messenger RNA in a cell-free system. 17 90

Guinea-pigs were immunized with different cells infected with vaccinia virus, herpes simplex virus type 1, herpesvirus saimiri, and the virus of vesicular stomatitis. Development of cellular immunity against these viruses was observed with transformation of blood and spleen lymphocytes and with the migration inhibition test using peritoneal exudate cells. Cellular immunity against vaccinia virus was first seen 6 days after the inoculation of cell-bound vaccinia virus by lymphocyte transformation. The avtivation of the vaccinia virus specific cellular immune response could be induced with tissue culturrus. Since infectious virus particles are not synthesized within this time period, it is likely that virus-induced antigens in the cell surface are active in production of cellular immunity. Vaccines from heterologous host cells were more effective inducers of an immune response than syngeneic cell cultures. For in vitro testing of cellular immunity to viruses, viral antigens could be used in both infective and inactivated form. Delayed hypersensitivity to viral antigens was always accompanied by immune reactions to the host cells used for virus propagation.
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PMID:Induction and in Vitro demonstration of cellular immunity to DNA and RNA viruses in guinea-pigs. 17 85

Interferon-treated cultures of Ly cells survived initial infection with high multiplicities of vesicular stomatitis (VSV) or herpes simplex virus (HSV). In the case of HSV, infectious virus and intracellular viral antigen were rapidly eliminated from the interferon-treated cultures, and the cells grew out to form apparently normal monolayers that could be cultured indefinitely. In the VSV-infected Ly cultures, virus titers remained at low levels in interferon-treated cells but after about 14 days rapidly rose and the culture was destroyed. If interferon was added to the medium on days 4 and 6 after infection, virus titers rapidly declined but again recovered and the cells were destroyed. If, however, interferon treatment was resumed 9 days after initial infection, detectable infectious VSV was eliminated from the medium. Several methods, including cocultivation and molecular hybridization, failed to demonstrate persistence of a significant portion of the VSV genome in these cultures.
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PMID:Fate of interferon-treated cells. 17 68

The results of treatment with LUPIDON achieved by 215 dermatologists with reference to a total number of 1059 cases are reported taking into account the controlled evaluation of questionnaires. Due to the considerable number of patients and physicians involved in this clinical investigation the presuppositions for objectiveness in respect of statistical evaluation were especially favourable. The results of treatment with LUPIDON--LUPIDON H and LUPIDON G proved to be of equal effectiveness--can be denoted as very positive because of the good or very good effects that could be observed in more than 80% of all the cases concerned. Such a therapeutically favourable result refers primarily to Herpes labialis, Herpes genitalis and Herpes eruptions infesting trunk and head; other types of herpes disease, for example Herpes glutealis or stomatitis aphthosa were only improved to about 60%. The compatability of LUPIDON was striking. The rate of side-effects was at 3%. Moreover, other series of data are given with the intention to inform about criteria such as: Frequency of localisations with regard to Herpes simplex diseases; distribution according to sex of patients being suffering from Herpes labialis and Herpes genitalis; distribution according to age; duration of Herpes simplex before starting a treatment with LUPIDON; accompanying skin diseases.
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PMID:[Results of treatment with the Herpes simplex antigen Lupidon H, resp. Lupidon G]. 17 31

In AKR mouse cells chronically infected with a murine leukemia virus, treatment with interferon for nine days resulted in sustained inhibition of extracellular production of murine leukemia virus but no inhibition of viral intracellular p30 antigen or of reverse transcriptase. Removal of interferon resulted in rapid reversal of these effects. Interferon-treated mouse L-cells were infected with high multiplicities of vesicular stomatitis virus or herpes simplex virus type 1. Infectious virus and intracellular viral antigen were rapidly eliminated from the interferon-treated cultures infected with herpes simplex virus. In cultures infected with vesicular stomatitis virus, titers of virus remained low in interferon-treated cells, but after about two weeks they rose rapidly and the cultures were destroyed. If treatment with interferon was reinstituted as late as nine days after primary infection, infectious vesicular stomatitis virus was eliminated, and there was no evidence for survival of the viral genome in these cultures. In the cultures infected with murine leukemia virus, inhibition of production of virus by treatment with interferon was possible, but the viral genome was not eliminated. In cells acutely infected with vesicular stomatitis virus or herpes simplex virus, however, the viral genomes were apparently eliminated from cultures treated with interferon.
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PMID:Persistence of the viral genome in interferon-treated cells infected with oncogneic or nononcogenic viruses. 18 Feb 9


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