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10.1128/JVI.02586-06

http://scihub22266oqcxt.onion/10.1128/JVI.02586-06
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C1900261!1900261!17376911
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suck abstract from ncbi


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pmid17376911      J+Virol 2007 ; 81 (11): 5527-36
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  • Generation and Characterization of a Recombinant Vesicular Stomatitis Virus Expressing the Glycoprotein of Borna Disease Virus? #MMPMID17376911
  • Perez M; Clemente R; Robison CS; Jeetendra E; Jayakar HR; Whitt MA; de la Torre JC
  • J Virol 2007[Jun]; 81 (11): 5527-36 PMID17376911show ga
  • Borna disease virus (BDV) is an enveloped virus with a nonsegmented negative-strand RNA genome whose organization is characteristic of mononegavirales. However, based on its unique genetics and biological features, BDV is considered to be the prototypic member of a new virus family, Bornaviridae, within the order Mononegavirales. BDV cell entry occurs via receptor-mediated endocytosis, a process initiated by the recognition of an as yet unidentified receptor at the cell surface by the BDV surface glycoprotein (G). The paucity of cell-free virus associated with BDV infection has hindered studies aimed at the elucidation of cellular receptors and detailed mechanisms involved in BDV cell entry. To overcome this problem, we generated and characterized a replication-competent recombinant vesicular stomatitis virus expressing BDV G (rVSV?G*/BDVG). Cells infected with rVSV?G*/BDVG produced high titers (107 PFU/ml) of cell-free virus progeny, but this virus exhibited a highly attenuated phenotype both in cell culture and in vivo. Attenuation of rVSV?G*/BDVG was associated with a delayed kinetics of viral RNA replication and altered genome/N mRNA ratios compared to results for rVSV?G*/VSVG. Likewise, incorporation of BDV G into virions appeared to be restricted despite its high levels of expression and efficient processing in rVSV?G*/BDVG-infected cells. Notably, rVSV?G*/BDVG recreated the cell tropism and entry pathway of bona fide BDV. Our results indicate that rVSV?G*/BDVG represents a unique tool for the investigation of BDV G-mediated cell entry, as well as the roles of BDV G in host immune responses and pathogenesis associated with BDV infection.
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