Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Monoclonal antibodies (MAbs) directed against herpes simplex virus (HSV)-coded glycoproteins gB, gC, gD and gE were employed in a an in vitro model of neuroinvasiveness using sensory neurons from rat dorsal root ganglion (DRG) cells. The neurons were cultured in at two-chamber system allowing infection via the neuritic extensions exclusively. The effects of 30 MAbs on viral replication of the encephalitis-derived HSV-1 strain 2762 and its less neuroinvasive variant 2762p11 were assayed in this model. One MAb reactive with gD gave a nine-fold reduction of the virus yields of both strains. One MAb directed against gB gave an enhanced virus yield of strain 2762, but not of the 2762p11 variant. Another gB-reactive MAb decreased the virus yield of strain 2762p11, but not of 2762 after neuritic infection. The findings indicate that an alteration of gB has occurred during the passage of the strain 2762. Mutants of the same strain were derived by infecting hybridomas producing MAb reactive with gB, gC, gD and gE, respectively. The gB hybridoma mutant showed a significantly lower neuroinvasiveness in the DRG model, and was non-virulent after snout infection of mice. We suggest that the structure of gB of the strain 2762 is of importance for the neuroinvasiveness of this strain.
Mol Cell Probes 1992 Feb
PMID:Mapping neuroinvasiveness of the herpes simplex virus type 1 encephalitis-inducing strain 2762 by the use of monoclonal antibodies. 131 21

Polymerase chain reaction (PCR) was prospectively performed with cerebrospinal fluid (CSF) from 51 patients whose CSF was available for analysis and was submitted for viral culture and/or herpes simplex virus (HSV) serology and 20 patients whose CSF was submitted exclusively to the Clinical Biochemistry Laboratory. Primers were used that flanked a 92 bp segment of the HSV DNA polymerase gene (35 cycles). Amplified products were electrophoresed on agarose gel, blotted onto nylon membrane, and probed with a 32P-labelled sequence internal to the primers. For nested PCR, 1 microliter of PCR product was amplified for an additional 35 cycles before electrophoresis and Southern blot analysis. Review of the clinical records revealed that 15 patients had central nervous system (CNS) infections. Specific HSV DNA sequences were detected in CSF specimens of three of the individuals [PCR(2), nested PCR(1)]. Two of these patients had disseminated HSV infection including encephalitis and one patient had aseptic meningitis. The diagnoses of the 12 patients with CNS infection who did not have HSV DNA detected in CSF included encephalitis [varicella-zoster virus (1), cytomegalovirus (1), Mycoplasma pneumoniae (1)], meningitis [Neisseria meningitidis (1), Coccidioides immitis (1), Enterovirus (1), aseptic meningitis (1)], varicella-zoster radiculitis (2), human immunodeficiency virus dementia (2), and transverse myelitis due to Epstein-Barr virus (1). Importantly, HSV DNA was also not detected in the CSF of the 36 patients who did not have CNS infection and 20 samples submitted exclusively to the Clinical Biochemistry Laboratory. Our findings demonstrate the utility of PCR as a rapid, non-invasive method for the routine laboratory diagnosis of CNS infection due to HSV.
Mol Cell Probes 1992 Oct
PMID:A prospective study of the polymerase chain reaction for detection of herpes simplex virus in cerebrospinal fluid submitted to the clinical virology laboratory. 133 47

On the base of two overlapping cDNA-clones of tick-borne encephalitis virus (TBEV) genome and synthetic DNA fragments full DNA-copy of the TBEV NS3 protein gene was constructed and expressed in the E. coli cells. It was demonstrated that the relatively low biosynthesis level of full-length NS3 protein in the bacteria was due to the toxicity of the N-terminal region of the protein, consisting of it's first 180 amino acid residues. A form of the gene with deletion of nucleotides coding for the toxic region (called NS3*) was constructed and effective bacterial product of NS3* protein was obtained. The panel of monoclonal antibodies to TBEV NS1 and NS3 proteins was generated. According to the results of experiments of the binding of the monoclonal antibodies 18B2 to the bacterial products of NS3 and NS3* genes it was concluded, that the antigenic determinant recognized by these antibodies was located between 174 and 236 amino acids of TBEV NS3 protein.
Mol Biol (Mosk)
PMID:[Expression of the gene for tick-borne viral encephalitis virus NS3 protein in Escherichia coli cells]. 150 65

The virus of infectious rhinotracheitis of cattle (BHV-1) causes the respiratory diseases, encephalitis, vulvovaginitis, abortions, etc. in sensitive animals. The attempts to differentiate the viral strains by virology and serology methods were unsuccessful. The restriction analysis makes possible to divide the strains into the three main groups designated BHV-1.1, BHV-1.2 and BHV-1.3. Majority of authors note the lack of correlation between the restriction pattern of DNA and the syndromes caused by the strains of the first and second groups while all the representatives of the third group were isolated in case of meningoencephalitis. The restriction analysis of BHV-1 strains isolated in the USSR by restriction endonucleases EcoRI, BamHI, HpaI and ClaI is presented. The obtained results show the absence of correlation between the restriction pattern of the strain and the syndrome caused by the viruses of all three groups. The representatives of the group BHV-1.3 that are not associated with the neurological syndrome are isolated for the first time.
Mol Gen Mikrobiol Virusol 1991 Apr
PMID:[Differentiation of strains of bovine infectious rhinotracheitis virus using restriction analysis]. 164 69

The collection of eight rat and mouse hybridomas secreting the high affinity monoclonal antibodies to glycoprotein E1 of the Venezuelan equine encephalomyelitis has been obtained. The antigenic structure of E1 protein has been studied with the use of these antibodies for the strains Trinidad, TC-83 and 230 of the virus. Antigenic map of glycoprotein E1 based on competition radioimmunoanalysis is proposed. Five sites are mapped including eight epitopes binding monoclonal antibodies. Antibodies to sites E1-1, E1-3 and E1-5 are crossreactive in interaction with the virus of Venezuelan equine encephalomyelitis, while antibodies to site E1-5 interact also with the virus of tick-borne encephalitis. Antibodies to site E1-1 possess the protective effect and lack the neutralizing effect in tissue cultures. Antibodies to all sites of E1 protein are devoid of ability to neutralize the Venezuelan equine encephalitis virus.
Mol Gen Mikrobiol Virusol 1991 Jun
PMID:[Study of the antigenic structure of the E1 glycoprotein of the Venezuelan equine encephalomyelitis virus using monoclonal antibodies]. 171 87

The 10466 nucleotide long sequence of the cDNA copy of the tick-borne encephalitis strain 205 viral genome has been determined. It includes the 5'-nontranslating region, the genes for structural as well as nonstructural proteins and the first 93 nucleotides of 3'-nontranslating region. The difference in amino acid sequences of structural and nonstructural proteins of strains 205. Sofjin and Neudoerfl of the tick-borne encephalitis virus and the nucleotide changes in 5'- and 3'-nontranslating of these strains are discussed.
Mol Gen Mikrobiol Virusol 1991 Apr
PMID:[Nucleotide sequence of genes and complete amino acid sequence of tick-borne encephalitis virus strain 205]. 185 76

Two possible forms of tick-borne encephalitis virus (TBE) gene NS1 (called NS1' and NS1) were constructed using two overlapping cDNA-fragments of TBE genome and synthetic DNA fragments. This genes were expressed in E. coli cells in expression vector pUR290 as individual proteins or fusion with bacterial beta-galactosidase. The proteins NS1 (Mw. 39 kDa), beta-galactosidase-NS1' (Mw. 162 kDa) and beta-galactosidase-NS1 (Mw. 155 kDa) were effectively synthesized under the Plgc-promoter induction conditions. Expression of NS1' gene results in the formation of two virus-specific proteins (Mw. 46 and 44 kDa). All bacterial analogs of NS1 protein fixed monoclonal and polyclonal antibodies specific to viral NS1.
Mol Biol (Mosk)
PMID:[Expression of gene coding for the NS1 protein of the tick-borne encephalitis virus in Escherichia coli cell]. 215 Dec 83

The nucleotide sequences of the cDNAs of the genes for the structural proteins C, preM, M and E of the tick-borne encephalitis viral strain 205 have been determined. The complete nucleotide sequence of the 5'-end nonstructural region of the viral genome has been studied for the first time. The difference in the amino acids sequences of the structural proteins from different strains (205, Sofiin and Neidorf) of the virus is discussed.
Mol Gen Mikrobiol Virusol 1990 Jan
PMID:[Tick-borne encephalitis virus: primary structure of DNA copies of the genes for strain 205 structural proteins]. 233 79

The recovery of RNA from postmortem (PM) brain tissues was quantified by molecular hybridization. RNA degradation rates postmortem were faster in mice with herpes encephalitis than with uninfected mice, but clear ribosomal peaks could be seen up to 72 hr after death. In a comparison between frontal cortex samples from neurologically normal and Alzheimer's disease cases a reduction in ribosomal, poly A, preproenkephalin, and preprosomatostatin RNA levels was observed in the Alzheimer's disease group. This general reduction may be influenced by the cause of death as well as the pathology.
Exp Mol Pathol 1986 Feb
PMID:Recovery and measurement of specific RNA species from postmortem brain tissue: a general reduction in Alzheimer's disease detected by molecular hybridization. 241 56

By employing a highly sensitive immunoassay method, concentration of the alpha subunit of GTP-binding protein, Go (Go alpha), recently shown to be localized mainly in nervous tissues and neuroendocrine cells, was determined in cerebrospinal fluids (CSF) of 192 patients with various neurological disorders and 50 control subjects. The results were compared with CSF levels of neuron-specific enolase (NSE) and S-100b protein (S-100b) in the same samples. Normal levels of Go alpha were 51.9 +/- 21.7 pg/ml. The levels of Go alpha, as well as NSE and S-100b, in CSF were enhanced in some patients with acute conditions, e.g., meningitis (48%), encephalitis (100%), and cerebral infarct (56%). In these disorders, cases with enhanced Go alpha levels were more frequent than those with enhanced NSE or S-100b. Three patients with encephalitis whose Go alpha levels were more than 1000 pg/ml all died; the remaining two patients with encephalitis and slightly elevated Go alpha levels had a good prognosis. Concentration of Go alpha in CSF correlated well with that of NSE but poorly with that of S-100b. However, cervical spondylosis and demyelinating diseases, CSF levels of Go alpha were generally lower than those of NSE or S-100b. These results suggest that Go alpha in CSF is a useful marker for monitoring patients with acute neuronal damage. Since these three proteins are distributed differently in the central nervous system, simultaneous determination of Go alpha, NSE, and S-100b levels in CSF might provide valuable information about the pathophysiology of neurological disorders.
J Mol Neurosci 1989
PMID:Elevated levels of the alpha subunit of GTP-binding protein Go in cerebrospinal fluid of patients with neurological disorders. 251 87


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