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Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Outbreaks of vesicular stomatitis, serotype New Jersey, during epidemics in the United States and northern Mexico, 1982-5, were examined by backward trajectories of winds to investigate spread and possible sources. The outbreaks selected for analysis did not involve introduction of disease by infected animals. The findings indicate that wind could have been responsible for carrying infection from northern Mexico to Arizona and New Mexico and thence to Colorado and Utah and on to Wyoming, Idaho and Montana. The results of these analyses are consistent with the findings from T1 RNAse fingerprinting of virus isolates from outbreaks during the epidemics. The arrival of the trajectories was associated with the passage of a front and rain or passage of a front alone or rain alone. At the time of the trajectories temperatures of 10 degrees C and higher were recorded at heights up to 2500-3500 m. Introduction by airborne particles would appear unlikely as it would have required a source of at least 10(5) infectious units per minute per animal. Vesicular stomatitis virus had been isolated from Simulium and Culicoides during the epidemic with amounts of virus from Simulium sufficient to suggest biological transmission. The possibility of Simulium infected with vesicular stomatitis virus being carried downwind to introduce disease is discussed in relation to the behaviour of Simulium and the pathogenesis of vesicular stomatitis in large animals.
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PMID:Trajectory analysis of winds and vesicular stomatitis in North America, 1982-5. 215 6

Feline lung monolayer cultures were treated with either a feline interferon (IFN) or one of two recombinant human alpha-IFNs and then challenged with feline herpesvirus 1 (FHV-1), feline calicivirus (F-9 strain), or vesicular stomatitis virus. Treatment with these IFNs reduced the viral yield for each of these three viruses as compared with that of control cultures. Vesicular stomatitis virus was more sensitive to each IFN than were FHV-1 or feline calicivirus F-9.
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PMID:Susceptibility of feline herpesvirus 1 and a feline calicivirus to feline interferon and recombinant human leukocyte interferons. 241 78

Preimplantation bovine ova were exposed in vitro to vesicular stomatitis virus, Indiana serotype, to document adherence of the virus to the zona pellucida. To determine the efficacy of this treatment, some of the ova were treated with trypsin after exposure to the virus. Vesicular stomatitis virus was isolated from 5 of 10 groups of zona pellucida-intact ova after 12 sequential washes without trypsin treatment. Vesicular stomatitis virus was also isolated from 4 of 11 groups of zona pellucida-intact ova after trypsin treatment.
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PMID:Trypsin treatment of bovine ova after in vitro exposure to vesicular stomatitis virus. 254 24

The course of vesicular stomatitis in cattle was investigated in 2 dairy herds (A and B) located in the southern San Joaquin Valley of California. Cattle were examined and specimens were obtained for virus isolation and for serologic survey for one year after an epizootic in December 1982. All 33 lactating cows selected for study had oral lesions, but only 19 (58%) were drooling or frothing around the mouth. Lesions on feet and teats were not observed. The healing time (longer than has been reported previously) for oral lesions ranged from 34 to 59 days. The mean serum neutralizing antibody titer for all cows tested in both herds 21 days after clinical signs were first observed was greater than 1:512. The mean titer decreased in the first 11 months after the epizootic, but remained greater than 1:128, and then increased during December 1983. Vesicular stomatitis virus/New Jersey strain was not isolated from 239 blood samples, 235 swab specimens of oral cavities, 38 swab specimens of oral epithelium, 206 urine specimens, or 232 fecal specimens collected from cows; however, it was isolated from tongue epithelium of 3 cows at 1, 4, and 21 days after signs of frothing were first noticed. For 20 lactating cows brought into dairy A during the epizootic, a mean time of 8.9 days elapsed between time of entry and appearance of clinical signs of vesicular stomatitis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vesicular stomatitis virus (New Jersey strain) infection in two California dairy herds: an epidemiologic study. 282 14

Vesicular stomatitis virus and encephalomyocarditis virus do not multiply in the majority of peritoneal macrophages freshly explanted from 4- to 8-week-old male or female mice. However, when peritoneal macrophages were cultivated in vitro for 3 to 5 days, these cells became permissive for both viruses. The loss of antiviral state in "aged" macrophages paralleled a significant decrease in the intracellular levels of (2'-5')oligo-adenylate synthetase activity. Although biologically active interferon was not detected in the nutrient medium of macrophage cultures, freshly harvested peritoneal cells could confer an antiviral state on monolayer cultures of mouse cells (aged macrophages, embryonic fibroblasts, and L cells) but not on heterologous chicken embryo, rabbit kidney, or human cells infected with vesicular stomatitis virus or encephalomyocarditis virus. The conferred antiviral state required at least 7 h to develop in target cells and was totally inhibited by the presence of antibody to mouse interferon alpha/beta but not to interferon gamma in the cocultures. Heterologous guinea pig and rabbit peritoneal cells could not transfer an antiviral state to target mouse cells. Donor peritoneal cells from mice preinjected with antibody to interferon alpha/beta could not transfer an antiviral state to target mouse cells. This ensemble of results indicating that freshly harvested peritoneal cells transfer interferon (which is responsible for inducing an antiviral state in susceptible mouse target cells) adds further experimental evidence that interferon is spontaneously expressed in normal mice and plays an important role in maintaining some host cells in an antiviral state.
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PMID:Mouse peritoneal cells confer an antiviral state on mouse cell monolayers: role of interferon. 300 78

The requirement of the presence of a nucleus for the replication of vesicular stomatitis virus and influenza virus has been examined by following the growth and development of these viruses in enucleate BS-C-1 cells. Vesicular stomatitis virus replicates normally in enucleate cells with the rate of production of infectious virus, the amount of virus-specific protein synthesis, and the type of proteins produced being essentially the same in nucleate and enucleate cells. Influenza virus does not replicate in enucleate cells, no virus gene products can be detected, and there is no inhibition of cellular protein synthesis.
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PMID:Virus replication in enucleate cells: vesicular stomatitis virus and influenza virus. 435 99

The in vivo synthesis of polycistronic transcripts of vesicular stomatitis virus in human amnion U cells and mouse L cells was detected by RNA blot hybridization. Within the molecular weight range resolved by this gel electrophoresis system, all possible combinations of sequentially linked messages were observed, as identified by their patterns of hybridization and their apparent molecular weights. Actinomycin D pretreatment of mouse L cells did not affect the frequency or size of polycistronic messages, nor did these differ between L cells and U cells. Vesicular stomatitis virus polycistronic transcripts were synthesized in vivo in a roughly uniform distribution, except for the NS-M dicistronic mRNA, which was much more frequent. Most of the polycistronic RNA species were found to be poly(A)+, but at least one, the tetracistronic molecule N-NS-M-G, was clearly poly(A)-. Analysis of RNA following treatment with RNase H in the presence of oligo(dT) indicated that the in vivo-synthesized poly(A)+ polycistronic species NS-M, M-G, and N-NS-M had poly(A) tracts at their 3' molecular termini but not internally at their intercistronic junctions.
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PMID:Detection of in vivo synthesis of polycistronic mRNAs of vesicular stomatitis virus. 615 26

First- and third-generation cloned progeny viruses were derived from clinical isolates of herpes simplex virus and examined for their sensitivities to human interferon by inhibition of plaque formation in Vero cells. The dose-response curves obtained with the first- and third-generation clones were similar to those obtained with the parental isolates, and both the parent and the clones showed similar sensitivities to interferon. These results suggest that clinical isolates of herpes simplex virus consist of a homogeneous population of virus particles with respect to interferon sensitivity. The dose-response curves obtained with herpes simplex virus demonstrated a shallower slope than those obtained with vesicular stomatitis virus. Vesicular stomatitis virus plaque formation as completely inhibited at high concentrations of interferon, whereas complete inhibition of plaque formation by herpes simplex virus did not occur at the highest concentration of interferon used. Cloned progeny were derived from plaques appearing in the presence of high concentrations of interferon. The dose-response curves and interferon sensitivities of these clones were similar to those of the parent and third-generation clone from which they were derived. There was no evidence for genetic heterogeneity with respect to interferon sensitivity.
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PMID:Response of cloned progeny of clinical isolates of herpes simplex virus to human leukocyte interferon. 615 4

Vesicular stomatitis virus (Indiana strain) will only grow in T lymphocytes which have been stimulated to undergo cell division. Evidence is presented that a considerable enrichment of the vesicular stomatitis virus-replicating T cells may be accomplished in the mouse spleen by passing the spleen cells over glass wool columns. By using this procedure experiments were performed to study the nature of the block in vesicular stomatitis virus replication in unstimulated (nonpermissive) versus mitogen-stimulated (permissive) splenic T cells. The results show that, as is the case in permissive T-cell lines, stimulated normal T cells allow the synthesis of the 42S virion ribonucleic acid.
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PMID:Replication of vesicular stomatitis virus in murine spleen cells: enrichment of the virus-replicating lymphocytes and analysis of replication restriction. 626 Jun 80

Vesicular stomatitis virus was extracted with 60 mM octylglucoside in the absence of salts and in the presence of 0.5 M NaCl. The resulting extracted virus particles were examined by electron microscopy, and the proteins present were identified by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Extraction in the absence of salts yielded subviral structures which we cell "skeletons" as originally suggested by Cartwright et al. (J. Gen. Virol. 7:19-32, 1970). The skeletons contained the viral N, M, and L proteins, but they lacked the glycoprotein (G) entirely. Morphologically, the skeletons resembled intact vesicular stomatitis virus but they were slightly longer and smaller in diameter. Like native vesicular stomatitis virus, skeletons were found to have lateral striations spaced 5.0 to 6.0 nm apart along the length of the structure. In contrast to extraction in the absence of NaCl, extraction of vesicular stomatitis virus with 60 mM octylglucoside in the presence of 0.5 M NaCl yielded highly extended viral nucleocapsids in which N was the predominant protein; no M or G proteins could be detected. These results support the view that the M protein is involved in maintaining the nucleocapsid in the compact form found in native virions.
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PMID:Role of the vesicular stomatitis virus matrix protein in maintaining the viral nucleocapsid in the condensed form found in native virions. 626 17


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