乙型肝炎表面抗原
病毒学
乙型肝炎病毒
外周血单个核细胞
分子生物学
生物
传染性
乙型肝炎病毒β前体
体外
病毒
突变体
乙型肝炎病毒DNA聚合酶
基因
生物化学
作者
María Cabrerizo,Javier Bartolomé,V. Carreño
标识
DOI:10.1046/j.1365-2893.2002.00367.x
摘要
summary . Previously, we identified a defective hepatitis B virus (HBV) which contains a 183 nucleotide deletion in the PreS1 region of the viral genome affecting the S gene promoter in sera from hepatitis B surface antigen (HBsAg)‐negative patients with serum HBV‐DNA. The aim of this study was to analyse the infectivity of this mutant. Peripheral blood mononuclear cells (PBMC) from a healthy donor were incubated with serum samples from 2 HBsAg‐negative patients with serum HBV‐DNA (infected with wild‐type and deletion mutant HBV), from an HBsAg carrier (infected with wild‐type HBV) and from a healthy donor. After 1 week, HBV‐DNA was detected by polymerase chain reaction (PCR) in all supernatants and cells incubated with the HBV‐DNA‐positive inocula. DNase and trypsin pretreatment confirmed intracellular localization of HBV‐DNA in cells. HBV‐RNA and covalently closed circular HBV‐DNA were also detected in PBMC, indicating that the viral DNA infecting these cells was transcriptionally active. Deletion mutant and wild‐type HBV were detected in the supernatants and cells infected with the two HBsAg‐negative sera, while only wild‐type HBV was detected in the supernatant and cells incubated with the serum from the HBsAg‐carrier. In conclusion, this HBV deletion mutant can infect, replicate and release viral particles in in vitro infected PBMC.
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