Summers J, Smith P M, Horwich A L
Department of Cell Biology, University of New Mexico School of Medicine, Albuquerque 87131.
J Virol. 1990 Jun;64(6):2819-24. doi: 10.1128/JVI.64.6.2819-2824.1990.
Primary duck hepatocytes were infected with a mutant duck hepatitis B virus defective in envelope protein but competent for viral DNA synthesis. Cells infected by this mutant accumulated higher levels of viral covalently closed, circular DNA (cccDNA) than those infected by wild-type virus. The accumulation of high levels of cccDNA was due to a failure of the mutant-infected cells to suppress de novo cccDNA synthesis compared with suppression by cells infected by the wild type. The envelope-defective virus failed to establish a persistent infection in vitro, possibly because of a virus-mediated cell death. Therefore, one or both viral envelope proteins are required for regulation of cccDNA synthesis and for maintenance of persistent infection in vitro.
将原代鸭肝细胞用一种包膜蛋白缺陷但能进行病毒DNA合成的鸭乙型肝炎病毒突变体感染。被这种突变体感染的细胞比被野生型病毒感染的细胞积累了更高水平的病毒共价闭合环状DNA（cccDNA）。高水平cccDNA的积累是由于与野生型感染的细胞相比，突变体感染的细胞未能抑制从头cccDNA合成。包膜缺陷病毒未能在体外建立持续感染，可能是由于病毒介导的细胞死亡。因此，病毒的一种或两种包膜蛋白对于调控cccDNA合成以及维持体外持续感染是必需的。
