Disease relevance of Encephalitis, Tick-Borne

• For this purpose, we used a series of plasmid constructs encoding different forms of the envelope glycoprotein E of the flavivirus tick-borne encephalitis virus [1].
• By the use of limited trypsin digestion of purified virions, we generated a membrane anchor-free and crystallizable form of the tick-borne encephalitis virus envelope glycoprotein E. It retained its reactivity with a panel of monoclonal antibodies, and only subtle structural differences from the native protein E were recognized [2].
• A UDG-deficient vaccinia virus vector carrying the tick-borne encephalitis (TBE) virus prM/E gene, termed vD4-prME, was constructed, and its potential as a vaccine vector was evaluated [3].
• Capsid protein C of tick-borne encephalitis virus tolerates large internal deletions and is a favorable target for attenuation of virulence [4].
• To investigate the influence of pre-existing antibodies against tick-borne encephalitis (TBE) or yellow fever (YF) viruses on dengue virus antibody test results, we examined sera from vaccinees and from individuals with previous TBE virus infection [5].

High impact information on Encephalitis, Tick-Borne

• The envelope glycoprotein from tick-borne encephalitis virus at 2 A resolution [6].
• A mutant of tick-borne encephalitis virus (TBEV) carrying a deletion mutation within the furin recognition motif of protein prM (changing R-T-R-R to R-T-R) was previously shown to be noninfectious in BHK-21 cells [7].
• Spontaneous mutations restore the viability of tick-borne encephalitis virus mutants with large deletions in protein C [8].
• Eight fatal cases of tick-borne encephalitis with an unusual hemorrhagic syndrome were identified in 1999 in the Novosibirsk Region, Russia [9].
• Adaptation of tick-borne encephalitis virus to BHK-21 cells results in the formation of multiple heparan sulfate binding sites in the envelope protein and attenuation in vivo [10].

Chemical compound and disease context of Encephalitis, Tick-Borne

• Treatment of tick-borne encephalitis (TBE) virus with Triton X-100 (TX-100), octylglucoside (OG) or cetyltrimethylammonium bromide (CTAB) caused dissociation of the virus envelope into dimers or monomers of the glycoprotein V3 [11].
• Several mutations were introduced into the putative serine protease domain of the tick-borne encephalitis virus NS3 protein and into a possible internal cleavage site within the protein [12].
• Tick-borne encephalitis (TBE) virus was crosslinked by dimethylsuberimidate (DMS) and the cleavable dimetyl 3,3'-dithiobispropionimidate (DTBP) [13].
• Affinity labelling with aldehyde-containing analogs of initiation substrates of nuclear fraction of tick-borne encephalitis virus (TBEV) infected cells results in a labelling of a single polypeptide with a molecular mass of 68 kDa which was immunologically identified as TBEV NS3 protein [14].
• Two randomized, double blind dose comparison studies were conducted in 595 children in Austria and Germany with an albumin-free and thiomersal-free tick-borne encephalitis (TBE) vaccine [15].

Biological context of Encephalitis, Tick-Borne

• A single amino acid substitution in envelope protein E of tick-borne encephalitis virus leads to attenuation in the mouse model [16].
• Location of immunodominant antigenic determinants on fragments of the tick-borne encephalitis virus glycoprotein: evidence for two different mechanisms by which antibodies mediate neutralization and hemagglutination inhibition [17].
• By the use of monoclonal antibodies we have recently defined eight distinct epitopes on the structural glycoprotein of tick-borne encephalitis (TBE) virus which differ with respect to location, function, or serological specificity (Heinz et al, Virology 126, 525-537, 1983) [18].
• Primers were designed from the consensus sequence of these regions and were used in a reverse transcription/polymerase chain reaction (RT/PCR) to amplify a region of the central european tick-borne encephalitis virus Kumlinge NS5 gene [19].
• To study the pathophysiology of tick-borne encephalitis (TBE), the kinetics of neopterin and beta 2 microglobulin (beta 2M) production were measured in sequential, cerebrospinal fluid (CSF) and serum samples in 133 patients with aseptic meningoencephalitis (TBE, n = 72; non-TBE, n = 61) [20].

Anatomical context of Encephalitis, Tick-Borne

• Hybridomas secreting antibodies to the structural glycoprotein of tick-borne encephalitis (TBE) virus were prepared by fusion of X63-Ag8/653 mouse myeloma cells with spleen cells from mice immunized with purified glycoprotein complexes of TBE virus [21].
• Three large batches were prepared of lyzed splenocytic leukocyte dialyzate from SPF outbred mice, immunized with a live attenuated virus from the tick-borne encephalitis (TBE) complex [22].

Gene context of Encephalitis, Tick-Borne

• Tick-borne encephalitis virus (TBEV) encodes an abundant, highly immunogenic nonstructural glycoprotein, NS1 [23].
• We carried out in vivo and in vitro studies with tick-borne encephalitis (TBE) virus to investigate the possible role of furin in this process as well as the functional consequences of prM cleavage [24].
• Because monkeys are not uniformly susceptible to tick-borne encephalitis, the protective properties of the vaccines were assessed by passive transfer of monkey sera to mice and subsequent challenge of the mice with RSSEV or CEEV [25].
• T7 DNA-dependent RNA polymerase can transcribe RNA from tick-borne encephalitis virus (TBEV) cDNA with SP6 promoter [26].
• The production of a vaccine against tick-borne encephalitis virus has been monitored using both polyclonal sera and a library of monoclonal antibodies [27].

Analytical, diagnostic and therapeutic context of Encephalitis, Tick-Borne

• Site-directed mutagenesis of the tick-borne encephalitis virus NS3 gene reveals the putative serine protease domain of the NS3 protein [12].
• The significance of IgG antibody levels determined by a binding assay (ELISA) was investigated as a surrogate marker for the presence of neutralizing and hemagglutination inhibiting antibodies in sera from individuals vaccinated against tick-borne encephalitis (TBE) [28].
• Efficacy of vaccination against tick-borne encephalitis (TBE) using an abbreviated immunization schedule was compared in 31 heart transplant recipients (age: 54.5 +/- 11.5 years, mean time after transplantation: 53.5 +/- 23.7 months) under cyclosporine-based immunosuppression and 29 controls [29].
• Detection of tick-borne encephalitis virus by sample transfer, plaque assay and strand-specific reverse transcriptase polymerase chain reaction: what do we detect [30]?
• Crosslinking of tick-borne encephalitis virus with dimethylsuberimidate followed by SDS-PAGE analysis yielded polymers of the core protein V2 and the viral glycoprotein V3, both in continuously decreasing amounts [31].

References