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)

The stability of nine viruses, Aujeszky, Sindbis, Vesicular Stomatitis, Newcastle Disease, Vaccinia, FMD, HCC, Reo and Teschen virus in drinking and surface water was investigated comparatively at temperatures of 9 and 15 degrees C as well as the influence of water factors like seasonal difference in temperature, pH value, hardness and sort of water. The results can be summarized as follows: 1. At temperatures of 9 to 15 degrees C the majority of the viruses remained stabil in natural water for an astonishing long time. 2. Starting with virus concentration of about 10(4) infectious units per ml Teschen, Vaccinia, Reo, HCC and ND virus could mostly be demonstrated in water longer than 200 days and FMD, Aujeszky, Vesicular Stomatitis and Sindbis virus for 20 to 50 days on average at 9 degrees C. The stability of the viruses investigated decreased in water in the named turn. 3. Based on these results it can be assumed that under natural conditions with very low virus content of some particles the labile viruses such as Toga, Herpes, Rhabdo and pH labile Picorna remain infectious in water for some days. They should not have any importance as water contaminants. More resistant viruses like Paramyxo may keep infectious for weeks and very stabile viruses such as Entero, Reo, Adeno and Pox viruses several weeks to months. 4. As to factors temperature, pH, hardness and sort of water-within the naturally differing range-only the temperature and only in the case of less resistant viruses showed significant influence on the virus stability in water.
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PMID:[Stability in drinking and surface water of nine virus species from different genera (author's transl)]. 1 60

Serological methods of mixed agglutination and indirect immunofluorescence showed the BGM/MV cell line to possess monkey antigens. As a means of further characterizing the species constitution of the BGM/MV cell line, the species specificity of viral-induced interferon from these cells, as well as the response of these cells to exogenous interferons, was determined. Low titers of spontaneously elaborated interferon capable of protecting monkey but not mouse cells were detected in BGM/MV culture fluids. Interferon induced by Newcastle disease virus infection of BGM/MV cells was capable of conferring an antiviral state on monkey and, to a lesser extent, on mouse cells. Exogenous interferons of both homologous (BGM/MV) and heterologous sources failed to confer an antiviral state on BGM/MV cells. BGM/MV cells were found to be partially refractive to superinfection with measles virus but freely replicated mumps and vesicular stomatitis virus.
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PMID:Characterization of an in vitro persistent-state measles virus infection: species characterization and interference in the BGM/MV cell line. 16 89

Specific immunity developed by mice against protozoan (Toxoplasma gondii and Besnoitia jellisoni) and bacterial (Listeria monocytogenes) infections was compared with nonspecific protection conferred by prior infections. The results indicated that homologous immunity protected mice from more than 10-5 LD50 of T. gondii or B. jellisoni, but from only 10-2 LD50 of L. monocytogenes. Heterospecific protection among these organisms was for 10-0.4 minus 10-1.2 LD50. In studies in hamsters specific immunity to protozoan (T. gondii and B. jellisoni) and viral (equine Herpesvirus type 1 and Oriboca virus) infections was compared with nonspecific protection conferred by prior infections with several heterospecific agents: T. gondii; B. jellison; equine Herpesvirus type 1; Oriboca, Ossa, vesicular stomatitis, yellow fever, and Newcastle disease viruses; L. monocytogenes; and the bacillus Calmette-Guerin strain of Mycobacterium tuberculosis. The results indicated that homologous immunity in hamsters was effective against 10-6 minus 10-7 LD50 of T. gondii, B. jellisoni, equine Herpesvirus type 1, or Oriboca virus. Prior infection with Newcastle disease virus protected (probably by interferon induction) against 10-3 LD50 of equine Herpesvirus type 1. Heterospecific protection among other agents was for less than 10 LD50. This insignificant heterospecific protection in infections in which cellular immunity plays a role suggests that both the induction phase and the expression phase are specific.
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PMID:Specific immunity and nonspecific resistance to infection: listeria, protozoa, and viruses in mice and hamsters,. 16 41

Synovial cell lines were established from patients with rheumatoid arthritis (RA) and from normal human embryos. High levels of hyaluronic acid (HA) were produced by some RA cell lines, some of which were partially or completely resistant to infection with Newcastle disease virus (NDV), vesicular stomatitis virus (VSV), and rubella virus (RV). Normal fetal synovial cells lines were susceptible to NDV, VSV, and RV. Infection with virus became possible after treatment of RA cells with hyaluronidase to depolymerize HA, and HA prevented infection of normal synovial cells with VSV. These results provide evidence that HA and not chronic or latent viral infection is responsible for the lack of susceptibility of RA synovial cells to certain viruses.
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PMID:Rubella and rheumatoid arthritis: hyaluronic acid and susceptibility of cultured rheumatoid synovial cells to viruses. 16 79

The production and effect of interferon in the virus-transformed cell line TGk1, originating from kidney cells of Testudo gracea were studied and compared to those in the primary cell culture. West Nile virus and Newcastle disease virus were used as inducers. Interferon production in TGk1 cells began 6 hr later than in the primary cell culture and reached the maximum 64 IU, 18 hr after virus inoculation. In the primary culture, interferon production increased till the 48th hr reaching a fourfold level (256 IU). A significant reduction of the antiviral effect of interferon against vesicular stomatitis virus but not against vaccinia virus was observed in the transformed cells. The decreased interferon production and effect in TGk1 cells is regarded as a consequence of the disturbance of the interferon regulatory mechanism taking place as a result of the virus-induced transformation.
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PMID:Interferon induction and action in transformed poikilothermic cells. 16 42

Peripheral blood leukocyte and spleen cell cultures derived from adult sheep and from third-trimester (107 to 145 days of gestation) and second-trimester (70 to 98 days of gestation) fetal lambs were examined for their ability to support viral replication and to produce interferon. Bluetongue virus, Herpesvirus hominis type 2, and Chikungunya virus failed to replicate in either leukocyte or spleen cell cultures derived from adult ewes or in cultures from second- or third-trimester fetal lambs. Similarly, peripheral blood leukocytes from adult sheep or third-trimester fetal lambs did not support the replication of Semliki Forest virus, vesicular stomatitis virus, Newcastle disease virus, or vaccinia virus. No major differences were observed in the ability of fetal and adult leukocytes to produce interferon in response to viral infection. In contrast, mean interferon titers induced by bluetongue virus, H. hominis type 2, and Chikungunya virus in spleen cells from second-trimester fetuses were 4- to 10-fold greater than those induced in spleen cells from adult ewes. Variations in interferon levels induced on separate occasions with cells from the same donor age group were observed. The antiviral substance induced in both the fetal and adult cell cultures fulfilled the usual criteria for characterization as interferon.
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PMID:Viral replication and interferon production in fetal and adult ovine leukocytes and spleen cells. 17 52

Disulfiram at concentrations between 0.1 and 0.3 mM inhibits the multiplication of Semliki Forest virus (SFV), fowl plague virus (FPV), Newcastle disease virus (NDV), vesicular stomatitis virus (VSV), and pseudorabies virus (PRV), when administered 1 hour before and during adsorption. There is, however, no inhibition of virus multiplication, when the drug is added after adsorption onto chick embryo cells. Disulfiram interferes neither with the receptors of the virus nor of erythrocytes, and it does not prevent virus adsorption. Possibly an early step in virus multiplication is affected by disculfiram. Infected cells once treated with the drug recover after some time of incubation in an ingibitor-free medium. The inhibitory state can be maintained, however, if relatively low doses of disulfiram are present in the culture medium also after adsorption. Disulfiram has no effect on macromolecular synthesis of the host cells. It has, however, a marked affect on membrane function. While virus multiplication is readily inhibited by disulfiram when chick embryo or BHK cells were investigated, virus multiplication in HeLa cells is almost resestant against the action of disulfiram.
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PMID:Effect of tetraethyl thiuram disulfide (disulfiram) on the multiplication of enveloped viruses. 17 61

A method is described for analysis of viral protein synthesis early after infection when minute amounts of viral proteins are effectively concealed by large amounts of produced host-specific proteins. The method is superior to a radioimmune assay, since all virus-induced proteins can be measured independent of their immunological reactivity. Host-specific protein synthesis can be suppressed by infection with fowl plague virus. Addition of actinomycin C 1.25 h postinfection does not prevent this suppression, but it does block effectively the formation of fowl plague virus-specific proteins. Such cells synthesize only small amounts of cellular proteins, as revealed by polyacrylamide electrophoresis. They can be superinfected with several different enveloped viruses, however, without significant diminution of virus yeilds. In pretreated cells the eclipse is shortened for Semliki Forest virus, Sindbis virus, and vesicular stomatitis virus, but prolonged for Newcastle disease virus. The onset of protein synthesis, specific for the superinfecting virus, could be clearly demonstrated within 1 h after superinfection. At this time, in cells superinfected with Semliki Forest virus, great amounts of NSP 75 (nonstructural protein; molecular weight, 75 X 10(3)) and reduced amounts of the core protein C could be deomonstrated. The precursor glycoprotein NSP 68 is followed by a new polypeptide, NSP 65: three proteins with molecular weights exceeding 100 X 10(3) were observed which are missing later in the infectious cycle. Similar results were obtained after superinfection with Sindbis virus. The formation of a new polypeptide with a molecular weight of about 80 X 10(3) was detected. After superinfection with vesicular stomatis virus or Newcastle disease virus the formation of new proteins, characteristic for the early stage of infeciton, was not observed.
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PMID:Inhibition of cellular protein synthesis by simultaneous pretreatment of host cells with fowl plague virus and actinomycin D: a method for studying early protein synthesis of several RNA viruses. 17 75

The effect of theophylline and adrenaline on the synthesis of interferon induced by the influenza B virus, strain Lee, in a chick embryo tissue culture was studied. Both preparation were found to decrease interferon synthesis when 5-day-old cultures were used; the inhibitory effect was increased when the two drugs were used together. The degree of inhibition of interferon production depended on a dose of the preparation; the inhibition was still present even when the drugs ere introduced several hours after the cells were infected with interferonogen. The treatment of one-day-old cultures with theophylline resulted in increase of interferon synthesis, whereas administration of adrenaline alone or together with theophylline did not affect the level of interferon synthesis. The drugs used produced no effect on the reproduction of the test-virus of vesicular stomatitis, Newcastle disease and Chickungunya viruses in chick embryo cells and influenza B virus in the developing chick embryos. The results obtained are discussed from the point of view of a possible influence of the intracellular adenosine 3',5-cyclic monophosphate level on the synthesis of virus-induced interferon.
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PMID:[Effect on drugs changing the intracellular level of adenosine 3',5'-cyclic monophosphate on interferon formation in chick embryo cells of different ages]. 17 23

Interferon production by leukocytes in culture was investigated in nine severely marasmic infants and 31 well-nourished controls. The production of interferon was induced with Newcastle disease virus and assayed in Vero cells challenged with vesicular stomatitis virus. Marasmic infants produced significantly less interferon than controls. It is suggested that the finding may be the result of a lymphocyte defect induced by malnutrition and could help to explain the increased frequency and severity of viral diseases in this condition.
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PMID:Decreased interferon production by leukocytes in marasmus. 18 Jul 90


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