Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Evidence was obtained indicating differences in the survival rate of Western equine encephalomyelitis virus after exposure to ultraviolet radiation and methyl methanesulfonate in commercial and leukosisfree chick embryo cells that differed in repair activity. The levels of spontaneous mutagenesis (on the basis of the yield of small palque variants of the encephalomyelitis virus) did not essentially change when the virus was passage in leukosis-free chick embryo cells, whereas an increase in the number of small palque variants was observed in the cells of commercial chick embryos. A 10-fold increase in the number of induced virus variants was observed in commercial chick embryo cells in experiments with methyl methanesulfonate as compared with the contorl, whereas the induction of virus variants was not noted in leukosis-free cells.
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PMID:Spontaneous and induced mutagenesis in Western Equine encephalomyelitis virus in chick embryo cells with different repair activity. 16 25

The complement fixation-inhibition (CFI) test was described for the detection of antibodies to arboviruses in bird sera. The CFI antibody present in bird sera inhibited the standard complement-fixation reaction of a reference complement-fixing antigen-antibody pair. Using reference antigens (St. Louis encephalitis, eastern equine encephalomyelitis, western equine encephalomyelitis, and yellow fever) prepared from infected mouse brains and reference antisera prepared in rabbits or horses, reproducible CFI antibody titers were obtained in artificially immunized chickens. Time-course studies on the CFI immune response in birds inoculated with live St. Louis encephalitis virus indicated that the CFI antibody was distinct from the antibody detected by the hemagglutination-inhibition test.
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PMID:Detection of arbovirus antibodies in avian sera by the complement fixation-inhibition test. 46 71

In mid-July, 1975, western equine encephalomyelitis (WEE) virus was isolated from mosquitoes collected in flooded areas of eastern North Dakota and western Minnesota. Inasmuch as clinical manifestations of WEE are usually observed in horses before human cases of encephalitis are recognized, surveillance of equine disease was initiated. Sixty-one practicing veterinarians from the are under surveillance reported 281 cases of WEE in horses from June through September, with peak incidence in late July. The high percentage of sero-positive, clinically normal, unvaccinated horses in one region suggested that many horses had developed non-clinical infections. The efficacy of vaccines used by the practitioners appears to have been execllent, as none of the horses vaccinated before the epizootic became ill during the period of surveillance. It was concluded that data collected from routine surveillance of encephalomyelitis in horses could be used to predict epidemics of WEE.
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PMID:Western equine encephalomyelitis in horses in the Northern Red River Valley, 1975. 87 43

Field studies were conducted in 1972 to determine the immunization status of equines along the Mexico, Arizona, and New Mexico borders. Interviews with horse owners were conducted along roads selected at random in the counties of Santa Cruz and Yuma, Ariz., and in Dona Ana County, N. Mex. At least 450 horse owners in each county were asked about the vaccination status of their animals, and information was taken on 1,260 animals. Blood specimens were obtained from every third equine, regardless of stated vaccination status, and tested for the presence of Venezuelan equine encephalitis (VEE), western equine encephalomyelitis (WEE), and eastern equine encephalomyelitis (EEE) neutralization antibodies. Serum samples were collected from 446 equines in the 3-county area; only 227 (50.7 percent) had both a history of VEE vaccination in 1971 (including 20 vaccinated in 1972) and serum neutralization antibody against VEE. Of the remaining 220 with no detectable neutralization antibody to VEE, 197 (89.5 percent) had a history of VEE vaccination in 1971 (including 5 revaccinated in 1972), 14 (6.4 percent) had no history of vaccination, and 9 (4.1 percent) had an unknown vaccination status. Eighty-two percent (160 of 1971) of the equines with a history of VEE vaccination and presence of dectectable WEE or EEE antibodies, or both, had no detectable levels of VEE antibody. Therefore, the results of this study suggest that the presence of WEE or EEE antibodies, or both, may suppress the development of dectable vaccine-induced VEE antibody response in the equine. As a result of this investigation, the U.S. Department of Agriculture, as an added precaution, recommended the revaccination of equines in areas of the United States bordering Mexico.
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PMID:Venezuelan equine encephalitis vaccination survey in Arizona and New Mexico, 1972. 87 11

Hyperimmunization with the tick encephalitis and Western horse encephalomyelitis viruses reproduced in the brain of albino mice, intensified the protein synthesis in the splenic tissue during the productive phase of the immunogenesis (the 7th day). An accumalation of protein, activation of aniuno-acyl-t-RNA-ligases, a reduction of the concehtration of some amino acids was noted, An analogous reaction was distinct in the tissue of the liver only when an intact brain suspension was used as an antigen. Formation of specific antibodies coursed more intensively after the administration of a more pathogenic virusof Western equine encephalomyelitis.
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PMID:[Metabolic features of the liver and spleen and antibody formation in animals following hyperimmunization with viral antigens]. 102 35

As a result of the continuing threat of Venezuelan equine encephalomyelitis (VEE), a study was made to determine if revaccination against VEE (TC-83 vaccine) was feasible and if revaccination could be incorporated into other routine vaccination practices. Of the horses given annual vaccination with bivalent western equine encephalomyelitis (WEE) and eastern equine encephalomyelitis (EEE) vaccine, 57% retained detectable serum-neutralizing (SN) antiboyd titers for VEE 18 months after the initial VEE vaccination was given. Of horses with no record of WEE-EEE vacinnation, 100% retained detectable VEE SN antibody titers over the same period. The VEE geometric mean titer was 25 times greater for horses not previously vaccinated against WEE-EEE than for horses given annual WEE-EEE vaccination at the time of VEE vaccination. In horses vaccinated against VEE 18 months previously, the geometric mean titer increased from 4 to 70 at 48 days after the intitial WEE-EEE vaccination. This increase indicated that similar antigenic factors for VEE are possibly present in bivalent WEE-EEE vaccine. In horses previously vaccinated against WEE-EEE and VEE, the best SN antibody response to VEE revaccination occurred when VEE vaccine was given simultaneously with the bivalent WEE-EEE vaccine. Of 150 serum samples tested by both the SN and the hemagglutination-inhibiton tests, agreement between positive reactions at greater than or equal to 1:10 was 70% for VEE, 81% for EEE, and 87% for WEE.
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PMID:A field study of persistence of antibodies in California horses vaccinated against western, eastern, and Venezuelan equine encephalomyelitis. 119 May 98

Midguts of two strains of the mosquito vector Culex tarsalis were examined by light and electron microscopy following infection with western equine encephalomyelitis virus. Infection of the highly susceptible Knight's Landing strain with high-titered blood meals resulted in pathologic changes in the midgut epithelium after 2-4 days of incubation; lesions included sloughing of epithelial cells into the lumen and necrosis of cells in situ. Infection of Knight's Landing strain mosquitoes with low-titered blood meals and infection of the less susceptible Fort Collins strain with high-titered blood meals did not result in a significant increase in detached luminal cells, with respect to uninfected controls. Sloughing of infected cells into the midgut lumen may contribute to modulation of the mosquito infection. Lesions in the midgut of Cx. tarsalis are inconsistent with traditional views that regarded arbovirus infections of mosquito vectors as non-pathologic. These findings demonstrate that mosquito pathology is not an oddity limited to the previously described interaction between Culiseta melanura and eastern equine encephalomyelitis virus, and suggest that alphaviruses in general may adversely affect their mosquito vectors in nature.
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PMID:Pathologic changes in the midgut of Culex tarsalis following infection with Western equine encephalomyelitis virus. 144 10

The receptor region for virus-cell interaction in Venezuelan equine encephalomyelitis (VEE) and Eastern equine encephalomyelitis (EEE) viruses was studied using a panel of 17 monoclonal antibodies (MCA). They were able to block agglutination of goose erythrocytes. The dominant role of glycoprotein E2 in the formation of viral receptor for EEE and VEE viruses was demonstrated. Competitive radioimmunoassay identified three antigenic sites in this region. These sites were also responsible for virus neutralization. MCAs to these sites protected outbred mice against lethal infection. The presence of a highly conservative region in VEE (site E2-3) and EEE (site E2a) which produced cross-reacting antibodies blocking hemagglutination of Western equine encephalomyelitis, Semliki Forest, Sindbis, Getah, Aura, Chikungunya, and Pixuna viruses was established. A hypothesis is suggested concerning the existence of similar regions for the entire alphavirus genus, and the role of this region in virus-cell interaction.
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PMID:[A monoclonal antibody study of the receptor area of the Venezuelan encephalitis virus]. 172 20

Eighteen equids were inoculated with eastern equine encephalomyelitis (EEE) and 18 equids with western equine encephalomyelitis (WEE) viruses to produce EEE virus- and WEE virus-immunized equids. Twelve surviving EEE virus-seropositive equids, 15 surviving WEE virus-seropositive equids, and 10 nonimmunized, seronegative equids (controls) were subsequently inoculated with an equine pathogenic (epizootic) strain of Venezuelan equine encephalomyelitis (VEE) virus to determine cross-protective immunity. Challenge infection produced 90% mortality in control (nonimmunized) equids, and 40% mortality in WEE virus-seropositive equids; all EEE virus-seropositive equids survived. Postchallenge exposure VEE viremia levels in EEE virus- or WEE virus-seropositive equids were lower than those in the 10 nonimmunized VEE virus-inoculated control equids. Plaque-neutralizing antibody responses to VEE virus in the EEE virus- and WEE virus-seropositive equids were similar in time of onset and titer to the antibody responses of nonimmunized equids. Neutralizing antibody to the third equine encephalomyelitis virus (either EEE virus or WEE virus) was detectable in 19 of 27 equids after inoculation with the challenge virus, VEE. Demonstration of cross-protective immunity between EEE or WEE virus and VEE virus in equids confirmed field observations made during the VEE epizootic in Texas in 1971.
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PMID:Cross-protective immunity between equine encephalomyelitis viruses in equids. 255 75

An enzyme immunoassay (EIA) was evaluated for its efficacy at detecting eastern equine encephalomyelitis (EEE) virus in avian blood and brain specimens. Preliminary analysis of blood from experimentally infected house sparrows and naturally infected whooping cranes showed that EEE antigen could be detected with the EIA. Polyclonal mouse antibodies were selected for antigen capture, and rabbit antibodies were selected for antigen detection. Overnight antigen incubation increased sensitivity. The lower limit of EEE antigen detection was 10(3.5) TCID50/ml for a stock of virus. Sensitivity was 10% (2/20) for antigen detection in the blood of chicks inoculated with EEE virus less than 24 hr earlier. At 24 and 48 hr after infection, sensitivity was 100% (10/10). Sensitivity and specificity of antigen detection were excellent (100% for both) in house sparrows experimentally inoculated with EEE, Highlands J (HJ), western equine encephalomyelitis (WEE), or St. Louis encephalitis (SLE) virus and bled at 24 hr intervals. Cross-reactivity was observed, however, with high concentrations (10(5.5) TCID50/ml) of HJ virus. EEE antigen was detected in avian blood by the EIA after infectious virus had declined to undetectable levels. The EIA is a useful alternative to virus isolation in cell culture for diagnosis or detection of EEE virus infections in birds. The test has the advantages of being simple, rapid, and capable of detecting antigen in the absence of infectious virus.
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PMID:Detection of eastern equine encephalomyelitis viral antigen in avian blood by enzyme immunoassay: a laboratory study. 301 Jul 53


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