The HBSP gene is expressed during HBV replication, and its coded BH3-containing spliced viral protein induces apoptosis in HepG2 cells

Yi Wei Lu, Tuan Lin Tan, Vincent Chan, Wei Ning Chen

Research output: Contribution to journalArticlepeer-review

21 Scopus citations

Abstract

The mechanisms of liver injury in hepatitis B virus (HBV) infection are defined to be due not to the direct cytopathic effects of viruses, but to the host immune response to viral proteins expressed by infected hepatocytes. We showed here that transfection of mammalian cells with a replicative HBV genome causes extensive cytopathic effects, leading to the death of infected cells. While either necrosis or apoptosis or both may contribute to the death of infected cells, results from flow cytometry suggest that apoptosis plays a major role in HBV-induced cell death. Data mining of the four HBV protein sequences reveals the presence of a Bcl-2 homology domain 3 (BH3) in HBSP, a spliced viral protein previously shown to be able to induce apoptosis and associated with HBV pathogenesis. HBSP is expressed at early stage of our cell-based HBV replication. When transfected into HepG2 cells, HBSP causes apoptosis in a caspase dependent manner. Taken together, our results suggested a direct involvement of HBV viral proteins in cellular apoptosis, which may contribute to liver pathogenesis.

Original languageBritish English
Pages (from-to)64-70
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume351
Issue number1
DOIs
StatePublished - 8 Dec 2006

Keywords

  • Apoptosis
  • BH3
  • HBSP
  • HBV replication

Fingerprint

Dive into the research topics of 'The HBSP gene is expressed during HBV replication, and its coded BH3-containing spliced viral protein induces apoptosis in HepG2 cells'. Together they form a unique fingerprint.

Cite this