It is yet to be established whether bornaviruses causes any overt disease in humans. For example, recent studies demonstrated the existence of an avian reservoir of diverse bornaviruses and provided evidence that bornaviruses are the etiologic agent for proventricular dilatation disease, a neuroinflammatory disease of psittacine birds. The natural host range, prevalence, and geographic distribution of BDV are broad. The type member is Borna disease virus (BDV), the causative agent of Borna disease, an often fatal neurological disease occurring mainly in horses and sheep in endemic regions of central Europe. Members of the Bornaviridae are enveloped with nonsegmented negative-stranded RNA genomes. ![]() These results suggest that G encoded by members of the Bornavirdae are class III VFPs (gamma-penetrenes). Structural models were established for BDV G based on the post-fusion structure of a prototypic class III VFP, vesicular stomatitis virus glycoprotein (VSV G). Proteomics computational analyses suggest that the structural/functional motifs that characterize class III VFP are located collinearly in BDV G. ResultsĬlass III viral fusion proteins (VFP) encoded by members of the Rhabdoviridae, Herpesviridae and Baculoviridae have an internal fusion domain comprised of beta sheets, other beta sheet domains, an extended alpha helical domain, a membrane proximal stem domain and a carboxyl terminal anchor. BDV G is post-translationally cleaved by the cellular subtilisin-like protease furin into two subunits, a 41 kDa amino terminal protein GP1 and a 43 kDa carboxyl terminal protein GP2. The BDV glycoprotein (G) is an extensively glycosylated protein that migrates with an apparent molecular mass of 84,000 to 94,000 kilodaltons (kDa). Borna disease virus (BDV) is the type member of the Bornaviridae, a family of viruses that induce often fatal neurological diseases in horses, sheep and other animals, and have been proposed to have roles in certain psychiatric diseases of humans.
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