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)

Enzyme-linked immunosorbent assays (ELISAs) were developed for detection of immunoglobulin G (IgG) and IgM antibodies to Venezuelan equine encephalomyelitis (VEE) virus in vaccinated and naturally infected humans. A total of 441 sera found negative for VEE antibodies by plaque reduction neutralization were examined by IgG ELISA and gave a 1.0% false-positive rate; no false-positives were found in the IgM ELISA. Sera with neutralizing antibody to western or eastern equine encephalomyelitis virus did not react with VEE antigen in the IgG ELISA. Sensitivity of the IgG ELISA was determined by testing 100 coded pre- and postvaccination human sera. Sixty-two were positive by ELISA; 58 of these 62 were also positive by neutralization tests, and 38 were negative by both tests. No neutralization-positive, ELISA-negative sera were found. Comparison of titers obtained by ELISA and neutralization tests indicated that 88% varied randomly by a fourfold dilution factor or less, while 61% were identical or varied only twofold. In sera obtained sequentially from 10 vaccinees and 5 naturally infected patients, both IgG and IgM antibodies appeared between 2 and 3 weeks after vaccination or onset of symptoms. The IgG and IgM antibody ELISAs described are rapid, specific, and sensitive indicators of VEE antibody status in vaccinated and naturally infected individuals.
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PMID:Enzyme-linked immunosorbent assay detection of immunoglobulins G and M to Venezuelan equine encephalomyelitis virus in vaccinated and naturally infected humans. 335 84

The biology, veterinary importance and control of certain Nematocera are described and discussed. Culicoides spp. (family Ceratopogonidae) transmit the arboviruses of bluetongue (BT), African horse sickness (AHS), bovine ephemeral fever (BEF) and Akabane. Some other arboviruses have been isolated from these species, while fowl pox has been transmitted experimentally by Culicoides. These insects are vectors of the parasitic protozoans Leucocytozoon caulleryi and Haemoproteus nettionis, and the parasitic nematodes Onchocerca gutturosa, O. gibsoni and O. cervicalis. They also cause recurrent summer hypersensitivity in horses, ponies, donkeys, cattle and sheep. Farm animals can die as a result of mass attack by Simulium spp., which are also vectors of Leucocytozoon simondi, L. smithi and the filariae O. gutturosa, O. linealis and O. ochengi. Venezuelan equine encephalomyelitis (VEE) and Rift Valley fever (RVF) have been isolated from simuliids, and vesicular stomatitis virus New Jersey strain has been replicated in Simulium vittatum. Simuliids are well known as vectors of O. volvulus, the cause of human onchocercosis (river blindness). The family Psychodidae includes the genera Phlebotomus and Lutzomyia (subfamily Phlebotominae), vectors of Leishmania spp. in humans, dogs and other mammals. Vesicular stomatitis virus Indiana strain has been regularly isolated from phlebotomine sandflies. Mass attack by mosquitoes can also prove fatal to farm animals. Mosquitoes are vectors of the viruses of Akabane, BEF, RVF, Japanese encephalitis, VEE, western equine encephalomyelitis, eastern equine encephalomyelitis and west Nile meningoencephalitis, secondary vectors of AHS and suspected vectors of Israel turkey meningoencephalitis. The viruses of hog cholera, fowl pox and reticuloendotheliosis, the rickettsiae Eperythrozoon ovis and E. suis, and the bacterium Borrelia anserina are mechanically transmitted by mosquitoes. These insects also induce allergic dermatitis in horses. They transmit several filarial worms of both animals and humans, and are of great medical importance as vectors of major human diseases, including malaria, yellow fever, dengue fever and many more diseases caused by arboviruses.
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PMID:Nematocera (Ceratopogonidae, Psychodidae, Simuliidae and Culicidae) and control methods. 771 9

A sensitive and specific colorimetric dot assay following polymerase chain reaction (PCR) method has been developed to detect 0.1 pg of eastern equine encephalomyelitis viral (EEEV) RNA. The assay is 250-fold more sensitive than analysis by electrophoresis and is based on converting a 291-nucleotide sequence of the viral coat protein amino terminus into a double-stranded DNA (dsDNA) and amplifying the DNA using a specific primer pair and PCR. The amplified complementary DNA (cDNA) is denatured adsorbed onto a nylon strip, baked, and detected with a digoxigenin-labeled probe. Dots with viral cDNA are stained dark red, whereas controls do not stain or stain lightly. The assay is very specific and sensitive and detects only EEEV. RNA of Venezuelan equine encephalitis, St. Louis encephalitis, Keystone, Flanders, Tensaw, and western equine encephalitis viruses were not detected. EEEV (Ten Broeck) RNA was detected at the 10-ng level, indicating that the prototype we used may have different nucleotides in the region where the primer pair binds. The PCR amplified EEEV cDNA that was 92% homologous to the consensus sequence of EEEV. The detection of EEEV in the liver of an infected Emu bird and in field-collected mosquitoes from Florida and Massachusetts that were analyzed concurrently as blind samples by tissue culture plaque assay and by PCR dot analysis proved that the assay is sensitive and can be used to detect infected mosquitoes. The assay can detect at least 1 infected mosquito in a pool of 1,000 uninfected mosquitoes.
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PMID:Sensitive and specific colorimetric dot assay to detect eastern equine encephalomyelitis viral RNA in mosquitoes (Diptera: Culicidae) after polymerase chain reaction amplification. 786 41

Immunoglobulin M (IgM) and G (IgG) capture enzyme-linked immunosorbent assays (ELISAs) were used as possible adjuncts to hemagglutination inhibition (HI) and virus neutralization (VN) tests to differentiate between reaction to recent exposure to eastern equine encephalomyelitis (EEE) virus and those due to prior vaccination. Serum samples were evaluated by the IgM-capture ELISA, and the results were compared with those of HI and VN tests. Of 381 serum samples, 51% (195 samples) were positive by HI test (> or = 1:40) and 54% (205 samples) were positive by VN test (> or = 1:10), but only 35% (132 samples) were positive by IgM-capture ELISA (> or = 1:100). With only a few exceptions, the sera with IgG ELISA titers had a VN titer of > or = 1:100. When EEE virus isolation and serology were compared, the EEE cases were divided into three categories: 1) peracute cases--the serum was negative for EEE IgM and IgG by the ELISA, negative for VN antibody, but HI antibody positive; 2) acute cases--IgM and HI antibody positive but negative for IgG and VN antibody; and 3) transitional cases--positive for IgM and IgG antibodies, HI titers of 1:40-1:160, and VN titers of > or = 1:100. IgM antibodies of EEE virus were monospecific and did not cross-react with western or Venezuelan equine encephalomyelitis viral antigens by the ELISA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diagnosis of eastern equine encephalomyelitis virus infection in horses by immunoglobulin M and G capture enzyme-linked immunosorbent assay. 801 79

The complete nucleotide sequence of a 1982 Florida strain of eastern equine encephalomyelitis (EEE) virus, and partial sequence of the nonstructural protein genes of western equine encephalomyelitis (WEE) virus, were determined. The EEE virus genome was 11,678 nucleotides in length, excluding the cap nucleotide and poly(A) tail, and the nucleotide composition was 28% A, 24% G, 25% C, and 23% U. The organization of both EEE and WEE virus genomes was like that of other alphaviruses and included a termination codon between the nsP3 and nsP4 genes. Codon usage for 10 of 20 amino acids was nonrandom in the EEE genome, and dinucleotide CpG-containing codons were underutilized in both genomes. The slight CpG deficiency was similar to that seen in other alphaviruses and plant viruses in the alphavirus-like group, but less than that of poliovirus and yellow fever virus. This slight deficiency may reflect adaptation for replication in both CpG-deficient vertebrates, as well as insects which do not have CpG-deficient genomes. Phylogenetic analyses using nonstructural protein amino acid sequences indicated that alphaviruses evolved from a common ancestor which existed a few thousand years ago. An intercontinental introduction of an ancestral virus from the Old to New World, or vice versa, probably resulted in two main extant groups: one includes New World (EEE and Venezuelan equine encephalitis) viruses, while the other includes Old World (Sindbis, Middelburg, O'nyong-nyong, Ross River, and Semliki Forest) viruses. The position of WEE virus in the phylogenetic trees indicated that, in addition to its capsid gene (C. S. Hahn et al. (1988) Proc. Natl. Acad. Sci. USA 85, 5997-6001), WEE virus acquired its nonstructural genes from an EEE-like ancestor during recombination.
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PMID:A comparison of the nucleotide sequences of eastern and western equine encephalomyelitis viruses with those of other alphaviruses and related RNA viruses. 803 Feb 17

Evolution of viruses in the eastern equine encephalomyelitis (EEE) complex was studied by analyzing RNA sequences and oligonucleotide fingerprints from isolates representing the North and South American antigenic varieties. By using homologous sequences of Venezuelan equine encephalomyelitis virus as an outgroup, phylogenetic trees revealed three main EEE virus monophyletic groups. A North American variety group included all isolates from North America and the Caribbean. One South American variety group included isolates from the Amazon basin in Brazil and Peru, while the other included strains from Argentina, Guyana, Ecuador, Panama, Trinidad, and Venezuela. No evidence of heterologous recombination was obtained when three separate regions of the EEE virus genome were analyzed independently. Estimates of the overall rate of EEE virus evolution (nucleotide substitution) were 1.6 x 10(-4) substitution per nucleotide per year for the North American group and 4.3 x 10(-4) for the Argentina-Panama South American group. Evolutionary rate estimates for the North American group increased over 10-fold (from about 2 x 10(-5) to 4 x 10(-4)) concurrent with divergence of two monophyletic groups during the early 1970s. The North and South American antigenic varieties diverged roughly 1,000 years ago, while the two main South American groups diverged about 450 years ago. Analysis of multiple strains isolated from an upstate New York transmission focus during the same years suggested that, in certain locations, EEE virus may be relatively isolated for short time periods.
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PMID:Evolution of alphaviruses in the eastern equine encephalomyelitis complex. 825 25

The hemagglutination (HA) domains of the Venezuelan equine encephalomyelitis (VEE) and the eastern equine encephalomyelitis (EEE) viruses providing the interaction of virions and red blood cells were studied with the use of a panel of 17 hemagglutination inhibition (HI) monoclonal antibodies (MAbs). A highly conserved domain (C domain) forming alphavirus-group-reactive MAbs was identified in the E2 protein of the VEE and EEE viruses. These MAbs inhibited HA of the western equine encephalomyelitis, Semliki Forest, Sindbis, Getah, Aura, Chikungunya and Pixuna viruses. The involvement of amino acid residues 59 and 232 in the formation of the C region was demonstrated by sequencing the gene encoding the E2 protein of three escape variants of the VEE virus.
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PMID:Analysis of the hemagglutination activity domains of the Venezuelan equine encephalomyelitis and eastern equine encephalomyelitis viruses. 858 35

Enzyme immunoassay (EIA) with sixty types of monoclonal antibodies (MAbs) was used to study cross-reactive epitopes on the attenuated and virulent strains of the Eastern equine encephalomyelitis (EEE) and Venezuelan equine encephalomyelitis (VEE) viruses. All three structural proteins of the EEE and VEE viruses were demonstrated to have both cross-reactive and specific antigenic determinants. The glycoprotein E1 of EEE and VEE viruses possesses three cross-reactive epitopes for binding to MAbs. The glycoprotein E2 has a cluster of epitopes for 20 cross-reacting MAbs produced to EEE and VEE viruses. Cross-reactive epitopes were localised within five different sites of glycoprotein E2 of VEE virus and within four sites of that of the EEE virus. There are no cross-neutralising MAbs to the VEE and EEE viruses. Only one type of the protective Mabs was able to cross-protect mice against lethal infection by the virulent strains of the VEE and EEE viruses. Eight MAbs blocked the hemagglutination activity (HA) of both viruses. Antigenic alterations of neutralising and protective sites were revealed for all attenuated strains of the VEE and EEE viruses. Comparative studies of the E2 proteins amino acid sequences show that the antigenic modifications observed with the attenuated strains of the VEE virus may be caused by multiple amino acid changes in positions 7, 62, 120, 192 and 209-213. The escape-variants of the VEE virus obtained with cross-reactive MAbs 7D1, 2D4 and 7A6 have mutations of the E2 protein at positions 59, 212-213 and 232, respectively. Amino acid sequences in these regions of the VEE and EEE viruses are not homologous. These observations indicate that cross-reactive MAbs are capable of recognising discontinuous epitopes on the E2 glycoprotein.
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PMID:Glycoproteins E2 of the Venezuelan and eastern equine encephalomyelitis viruses contain multiple cross-reactive epitopes. 897 33

Part of WEE virus (strain 16310-5614) genome coding for the nucleocapsid (C) protein was cloned and sequenced in two independent clones. The C gene of WEE virus is composed of 77 nucleotides, both for the BFS and 16310 strains, and is 48, 24, 33, 15, 3, and 3 nucleotides shorter than that of Venezuelan equine encephalomyelitis (VEE), Semliki Forest, Ross River, Sindbis, O'Nyong-Nyong, and Eastern equine encephalomyelitis (EEE) viruses, respectively. It contains 16 nucleotide changes in comparison with the BFS-1703 strain, four of which are significant: Ser57(BFS)-->Ala(16310), Gly63-->Cys, Lys74-->Glu, Gly97-->Trp. Amino acid composition, charges, hydropathic profiles, and location of potential functional sites in C proteins of the heretofore studied alphaviruses have been compared. High positively charged N-domain of the nucleocapsid is the most variable in all alphaviruses and is characterized by an irregular secondary structure due to high Pro content (25.5%). Positively charged Lys (10.8% of total) and Arg (6.9% of total) are presented 18 and 11 times, respectively, in the N-domain of WEE virus (16310) protein, and clusters thereof possibly form the initial sites for interaction with RNA. Only Sindbis virus (HRSP and Ock) nucleocapsids do not contain Cys, while others do contain several residues. This part of C protein includes overlapping nuclear transport signals predicted for several cellular proteins and repeated 4, 7, and 2 times in WEE, EEE, and Sindbis viruses, respectively. There is a highly conservative region (96-113 as residues) in the C protein structure of all studied alphaviruses, which potentially binds to a large ribosomal subunit as it was shown for Sindbis virus by Wengler et al. (1992), and a consensus motif K/R95-P-X-K/R-X-R-M could be a main part of the nucleoprotein ribosome binding site. The W186HHGAVQ (WEE virus) is absolutely conservative for all alphaviruses and with the invariant Asn222 could have a common function, including C protein lateral interaction (Choi et al., 1991). The origination of WEE virus C protein from EEE virus is confirmed by very high (92.7%) similarity of this protein's C domain in the WEE/EEE pair and low (64.8%) in the WEE/Sindbis pair. Determination of C gene and protein type in the Sindbis/WEE virus serocomplex might be useful in the differential identification of this virus group.
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PMID:[Comparative analysis of primary structure of nucleocapsid protein from Western equine encephalomyelitis virus and other alphaviruses]. 899 81

Mice develop a fatal encephalomyelitis after infection with the Trinidad donkey strain of Venezuelan equine encephalitis (VEE) virus. Adult mice were inoculated intraperitoneally with VEE virus and the brains were examined at different time points. Morphological changes were assessed by histological staining. VEE virus antigen was detected with immunoperoxidase staining, and DNA fragmentation was evaluated in situ using the terminal deoxynucleotidyl transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) method. VEE antigen was found in many areas of the brain and it was prominent in neurons. There were mild associated inflammatory changes. DNA fragmentation was demonstrated in many of these areas using TUNEL. In areas with TUNEL staining, morphological neuronal changes ranged from nuclear chromatin condensations to nuclear and cellular fragmentation, which are characteristic of apoptosis. There is strong morphological and biochemical evidence of apoptotic cell death in this experimental model of VEE virus infection.
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PMID:Apoptotic cell death is an important cause of neuronal injury in experimental Venezuelan equine encephalitis virus infection of mice. 911


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