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- W2361844103 abstract "Objective To investigate the pathogenecity of truncated large surface proteingenerated by 458-1308nt spliced variant of HBV genome. Methods Substituted the initial codon of PreS2 and S region from ATG to ACG in full-length (accession number: AY206390, 3215bp) and 458-1308nt spliced variant(accession number AY238972, 2366bp) of HBV DNA by means of site-directed mutagenesis. Amplified the coding region for truncated large surface protein (LS-splice) and amino-terminal 276 amino acids (LS 276 ) using mutated 458-1308nt HBV DNA as the template, and amplified the coding region for full-length large surface antigen (LS) using mutated full-length HBV DNA as the template. Cloned the amplified fragment to eukaryotic expression vector pCDNA3.1 /Hyg(-) separately and transfected the recombinant vector to HepG2 cell and Chang cell lines by LipofectAMINE. Detected the cytoplasm vacuolization and apoptosis by routine hematoxylin-eosin staining and FACS respectively. Results Recombinant vector expressing LS, LS 276 and LS-splice repectively could cause the cytoplasm vacuolization both in HepG2 and Chang cell. In addition, LS could induce the apoptosis both in HepG2 and Chang cell, meanwhile, such effects vanished as to LS 276 and LS-splice. Conclusion Truncated large surface protein generated by 458-1308nt spliced variant of HBV genome was liver-pathogenic, and the pathogenesis was correlated with its amino terminal 276 amino acids. This type of spliced variant may be closely related with the pathogenesis of HBV." @default.
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- W2361844103 date "2004-04-30" @default.
- W2361844103 modified "2023-10-12" @default.
- W2361844103 title "Cellular vacuolization induced by truncated large surface antigen of hepatitis B virus due to pregenomic RNA splicing" @default.
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