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)

Infection of animal cells by vesicular stomatitis virus (VSV) results in inhibition of translation of cellular mRNA. We showed previously that, in BHK cells infected by the Glasgow isolate of VSV Indiana, this is due to competition during the initiation step of protein synthesis of viral and cellular mRNA for a constant, limiting number of ribosomes. We show here that infection of the same cells with the San Juan isolate of VSV resulted in a more rapid shutoff of host protein synthesis and that this was paralleled by a more rapid accumulation of viral mRNA. Extending our conclusion that shutoff is due to mRNA competition, we show further that the average size of polysomes translating viral and cellular mRNA was threefold smaller in cells infected by VSV San Juan than by VSV Glasgow, which, in turn, was about one-half that of uninfected cells. In all cases, cellular and viral mRNA's which encoded the same-sized polypeptides were found on the same-sized polysomes, a result indicating that the efficiency of translation of both types of mRNA's is about the same in the infected cell. Also, there was no preferential sequestration of viral or cellular mRNA's in ribonucleoprotein particles. Additional correlations between the levels of viral mRNA's and the inhibition of protein synthesis came from studies of three other wild-type VSV strains and also from studies with Vero and L cells. In particular, the rate of shutoff of L-cell protein synthesis after infection by any VSV isolate was slower than that in BHK cells, and this was correlated with a slower rate of accumulation of viral mRNA. VSV temperature-sensitive mutants which synthesized, at the nonper-missive temperature, no VSV mRNA failed to inhibit synthesis of cellular proteins. Stanners and co-workers (C. P. Stanners, A. M. Francoeur, and T. Lam, Cell 11:273-281, 1977) claimed that VSV mutant R1 inhibited synthesis of L cell protein synthesis less rapidly than did its parent wild-type strain HR. They concluded that this effect was due to a mutation in an unspecified VSV protein, "P." We found, in both L and BHK cells, that R1 infection resulted in a slightly slower inhibition of cellular mRNA translation than did HR infection and that this was correlated with a slightly reduced accumulation of VSV mRNA. The level of VSV mRNA, rather than any specific VSV protein, appeared to be the key factor in determining the rate of shutoff of host protein synthesis.
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PMID:Vesicular stomatitis virus mRNA and inhibition of translation of cellular mRNA--is there a P function in vesicular stomatitis virus? 626 24

Three defective interfering (DI) particles of vesicular stomatitis virus (VSV), all derived from the same parental standard San Juan strain (Indiana serotype), were used in various combinations to infect cells together with the parental virus. The replication of their RNA genomes in the presence of other competing genomes was described by the hierarchical sequence: DI 0.52 particles greater than DI 0.45 particles less than or equal to DI-T particles greater than standard VSV. The advantage of one DI particle over another was not due simply to multiplicity effects nor to the irreversible occupation of limited cellular sites. Interference, however, did correlate with a change in the ratio of plus and minus RNA templates that accumulated intracellularly and with the presence of new sequences at the 3' end of the DI genomes. DI 0.52 particles contained significantly more nucleotides at the 3' end that were complementary to those at the 5' end of its RNA than did DI-T or DI 0.45 particles. The first 45 nucleotides at the 3' ends of all of the DI RNAs were identical. VSV and its DI particles can be separated into three classes, depending on their terminal RNA sequences. These sequences suggest two mechanisms, one based on the affinity of polymerase binding and the other on the affinity of N-protein binding, that may account for interference by DI particles against standard VSV and among DI particles themselves.
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PMID:Interference among defective interfering particles of vesicular stomatitis virus. 628 14

Three hundred seventy-nine virus isolates were obtained from mosquitoes collected and sentinel hamsters exposed in coastal Ecuador from 1974 to 1978. These included four alphaviruses [Venezuelan equine encephalitis 1B (1), Venezuelan equine encephalitis 1D (35), western equine encephalitis (1) and eastern equine encephalitis (4)]; two flaviviruses [St. Louis encephalitis (3) and Naranjal (6)]; 11 bunyaviruses [Maguari (243), Playas (3), Vinces (33), Turlock (2), Abras (5), Babahoyo (3), Acara (2), Guajara (3), San Juan (6), Pueblo Viejo (3), 18 unspecified Gamboa serogroup viruses, Palestina (7)]; and one vesiculovirus (vesicular stomatitis New Jersey). All but Venezuelan equine encephalitis virus were new to Ecuador, and Naranjal (serogroup B), Playas (Bunyamwera serogroup), Vinces (serogroup C), Abras and Babahoyo (Patois serogroup), San Juan and Pueblo Viejo (Gamboa serogroup) and Palestina (Minatitlan serogroup) are newly recognized viruses. These isolates have enabled us to 1) expand our knowledge of the geographic distribution of recognized viruses, 2) expand our knowledge of the members of certain serogroups and 3) establish two new serogroups (Gamboa and Minatitlan).
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PMID:Identification of hitherto unrecognized arboviruses from Ecuador: members of serogroups B, C, Bunyamwera, Patois, and Minatitlan. 630 29

We have studied the effects of inhibiting the initial steps in processing of asparagine-linked oligosaccharides on the formation of vesicular stomatitis virus (VSV). Our data show that conditions which prevent the removal of glucose can block the growth of this virus. Our conclusion that inhibition of VSV synthesis is due specifically to an effect on the ability of the virus glycoprotein, G, to mature to a correct functional conformation is based on the following observations: (i) two drugs, deoxynojirimycin and castanospermine , both of which selectively inhibit the processing glucosidases, affected virus growth; (ii) only one of the two strains (San Juan and Orsay ) of VSV tested was affected and that strain, VSV(San Juan), is known to have a G protein highly sensitive to alterations in oligosaccharide structure; (iii) the effect was to make the formation of VSV(San Juan) temperature-sensitive, a result previously observed with alterations in the oligosaccharides on G protein; (iv) a cell variant missing glucosidase II activity also became temperature-sensitive in its ability to produce VSV(San Juan) but not VSV( Orsay ). Although inhibition of glucosidase activity by 1- deoxynojirimycin caused a 10-fold drop in virion formation, transport of G protein to the plasma membrane was not altered. The growth of VSV(San Juan) at 40 degrees C was not affected when subsequent steps in the processing pathway were blocked. These data indicate that by the time the glucose residues are removed G has attained a stable conformation.
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PMID:The formation of vesicular stomatitis virus (San Juan strain) becomes temperature-sensitive when glucose residues are retained on the oligosaccharides of the glycoprotein. 633 65

A novel nucleoside analog, 8-chloro-7-deazaguanosine (8-Cl-7-dzGuo), was evaluated for anti-RNA virus activity in rodents in parallel with the related compound 7-deaza-7-thia-8-oxoguanosine (7-dzTOGuo). Half-daily intraperitoneal (i.p.) doses of each substance administered 24 and 18 h prior to i.p. virus challenge protected the majority of mice infected with banzi, encephalomyocarditis, San Angelo, and Semliki Forest viruses at doses of 25, 50 and 100 mg/kg/day. These compounds at 100 mg/kg/day also protected most suckling rats infected intranasally with rat coronavirus. However, no survival benefit was afforded to treated mice infected intranasally with vesicular stomatitis virus. 8-Cl-7-dzguo was orally active against Semliki Forest virus in mice at 200 and 400 mg/kg/day, whereas 7-dzTOGuo is reported to not be effective orally. In uninfected mice, the two compounds induced similar amounts of interferon following i.p. injections. Interferon was induced by oral treatments with 8-Cl-7-dzGuo but not with 7-dzTOGuo. Fifty percent acute lethal doses to uninfected mice treated i.p. in half-daily doses for one day with 7-deazaguanosine (7-dzGuo), 7-dzTOGuo, and 8-Cl-7-dzGuo were 400, 600 and > 1600 (no mortality at this dose) mg/kg/day, respectively. Daily, i.p. treatments for 14 days with these substances (100 mg/kg/day) showed 7-dzGuo as 100% lethal and the other two substances as not toxic. By virtue of reduced toxicity and oral bioavailability, 8-Cl-7-dzGuo appears to have the greatest clinical potential as an interferon-inducing antiviral agent.
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PMID:Broad-spectrum activity of 8-chloro-7-deazaguanosine against RNA virus infections in mice and rats. 760 16

The matrix (M) protein of vesicular stomatitis virus (VSV) plays a central role in virus assembly by binding the nucleocapsid core to the viral envelope during the budding process. A small percentage of M protein molecules are phosphorylated in vivo, but the role of phosphorylation in M protein function is unknown. Using limited proteolysis, we previously determined the sites of in vivo phosphorylation for VSV M protein to be Thr 31 (and possibly Ser 32) and a site N-terminal to position 19 (Ser 2, Ser 3, or Ser 17) (P. E. Kaptur et al., J. Virol. 66, 5384-5392, 1992). M protein mutants were constructed using site-directed mutagenesis by substituting Ala for Ser or Thr at these sites in the M gene of the San Juan strain of VSV. One mutant had substitutions at the major in vivo phosphorylation site(s) at positions 31 and 32 (M31.32) while two others had additional substitutions at positions 2 and 3 (M2.3.31.32) or at position 17 (M17.31.32). Mutant M proteins were expressed in BHK cells using the vaccinia/T7 system, radiolabeled with 32Pi, and then analyzed for 32P content by PAGE and autoradiography. The data show that the site of phosphorylation near the N-terminus is at Ser 2 or 3 and not Ser 17. Further, Ser 38 was not phosphorylated. Mutation of the major phosphorylation site enhanced phosphorylation at alternative sites in the M protein C-terminal to amino acid 43 and at Ser residues 2 and 3. Mutant M proteins were tested for their ability to complement growth of the temperature-sensitive M protein mutant virus tsO23 at the nonpermissive temperature. Mutant M2.3.31.32 was further tested for its ability to assemble into VSV-defective interfering (DI) particles, using a replication system in which the DI genome and all five VSV proteins were expressed from plasmid DNA. Assembly of tsO23 virions or DI particles in the presence of mutant M proteins was similar to that observed for wild-type M proteins. These data indicate that phosphorylation of M protein at the major in vivo sites is not essential for virus assembly.
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PMID:Assembly functions of vesicular stomatitis virus matrix protein are not disrupted by mutations at major sites of phosphorylation. 785 2

As the scope of the acquired immunodeficiency syndrome (AIDS) epidemic grows to include increasingly larger proportions of heterosexual adults and children, there has also been a change in the severity of human immunodeficiency virus (HIV)-related periodontal conditions at one San Francisco clinic. The cases of HIV-associated gingivitis, now called linear gingival erythema, HIV-associated periodontitis (or necrotizing ulcerative periodontitis), and necrotizing stomatitis have been less severe, despite an increase in overall HIV caseload. No clear basis for this trend has been established, but possible explanations include: biased population samples, increased immunosuppression as the disease matures, use of antimicrobial therapy, or a change in patient demographics. Several studies have failed to identify a single causative organism. This article presents a review of HIV-related periodontal complications and points out that the condition can be treated with local and systemic antibiotics and that dental professionals throughout the world can expect a tremendous increase over the next several years in HIV-infected patients with special clinical complications.
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PMID:Periodontal complications of HIV infection. 803 7

A reverse transcription polymerase chain reaction (RT-PCR) procedure is described for the detection of marine caliciviruses including vesicular exanthema of swine virus (VESV), San Miguel sea lion virus (SMSV), bovine Tillamook virus (BCV Bos-1) and caliciviruses (CV) isolated from dolphin (Cetacean CV), gorilla (Primate CV) and rattlesnake (Reptile CV) using primers (1F and 1R) designed from the capsid-coding region of the viral genome. These primers were compared with those described by Neill, J.D. and Seal, B.S., 1995: Development of PCR primers for specific amplification of two distinct regions of the genomes of San Miguel sea lion and vesicular exanthema of swine viruses, Mol. Cell. Probes 9, 33-38 (Hel1/Hel2), which had been designed from the 2C-like region of the calicivirus genome. Both sets proved to be extremely useful diagnostic tools for all of the known marine calicivirus serotypes with the exception of three: SMSV-8 and -12 and mink CV suggesting that these three caliciviruses may belong to a different group. Neither of the two primer sets reacted with strains of the vesicular disease viruses of foot-and-mouth disease (FMD), swine vesicular disease (SVD) or vesicular stomatitis (VS) nor with two feline caliciviruses (FCV). The 1F/1R primer set has the advantage over the Hel1/Hel2 set in that it generates a larger PCR product for nucleotide sequence investigations and so provides greater opportunity for identifying molecular differences between the viruses.
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PMID:Development of a reverse transcription polymerase chain reaction procedure for the detection of marine caliciviruses with potential application for nucleotide sequencing. 1050 17

The characterization of an orf virus (OV) isolated from skin lesions of a goat kid with severe, persistent, proliferative dermatitis, and designated orf virus-San Angelo 2000 (OV-SA00) strain, is described. The identity of OV-SA00 was confirmed by a combination of methods, including electron microscopy, amplification of specific fragments of viral DNA by polymerase chain reaction, restriction enzyme analysis of viral DNA and gene sequencing. Restriction endonuclease analyses of viral DNA and the protein profile studied by Western blot revealed differences between OV-SA00 strain and the profiles of other OV strains that have been published. The restriction enzyme profile of OV-SA00 was also different from the orf virus vaccine (OV-V) strain used to vaccinate this kid. Comparison of the nucleotide and deduced amino acid sequences indicated that OV-SA00 is closely related to OV-V strain, the Scottish OV strains orf11 and MRI Scab, and the human OV-CE/Shoe strain and more distant to bovine papular stomatitis virus (BPSV) reference strain and the pseudocowpox virus (PCPV)-MNV/Till strain. These results indicate that OV-SA00 is a strain of OV rather than a different parapoxvirus. Further studies are necessary to determine if the severity of orf-induced lesions in this goat kid was the result of individual host susceptibility factors.
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PMID:Characterization of a North American orf virus isolated from a goat with persistent, proliferative dermatitis. 1278 65

This descriptive study assessed the self-reported medications taken by 1,163 European-American and Mexican-American community-dwelling adults (age range 32 to 81 years of age) from the Oral Health: San Antonio Longitudinal Study of Aging (OH:SALSA) sample and reports on the potential oral side effects (OSE) of their medications. Data collection included sociodemographic characteristics, number of prescription and non-prescription drugs, and frequency of potential OSE. Medications were checked in three drug references, and all potential OSE were classified into 16 major categories. The mean number of medications taken per subject was 2.7. Persons 65 years or older, females, European Americans, and suburban residents reported taking more drugs than their counterparts. There was no difference in the number of drugs taken due to income or education (p>0.05). The Spearman rank order correlation between age and number of medications was 0.30 (p<0.001). The most frequent potential OSE was dry mouth in 664 subjects (57%), followed by bleeding in 456 (39%), alteration in taste of 389 (33%), and stomatitis in 331 (28%). The distribution of subjects with respect to number of potential OSE was: none, 20%; 1 to 2, 24%; 3 to 4, 26%; 5 to 6, 14%; and 7 or more, 16%. Many older community-dwelling persons may be at risk for multiple oral complications due to medications they are taking.
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PMID:Exposure to the oral side effects of medication in a community-based sample. 1677 89


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