Altered DNA Mutation Spectrum in Aflatoxin B1-Treated Transgenic Mice That Express the Hepatitis B Virus X Protein
AUTOR(ES)
Madden, Charles R.
FONTE
American Society for Microbiology
RESUMO
Humans chronically infected with hepatitis B virus (HBV) are at further risk of liver cancer upon exposure to dietary aflatoxin B1 (AFB1), a carcinogenic product of the mold Aspergillus flavus. For the present study, we utilized double-transgenic mice (ATX mice) that express the HBV X protein (HBx) and possess a bacteriophage lambda transgene to evaluate the in vivo effect of HBx expression on AFB1-induced DNA mutations. The expression of HBx correlated with a 24% increase in mutation frequency overall and an approximately twofold increase in the incidence of G/C-to-T/A transversion mutations following AFB1 exposure. These results are consistent with a model in which expression of HBx during chronic HBV infection may contribute to the development of hepatocellular carcinoma following exposure to environmental carcinogens.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=136763Documentos Relacionados
- Hepatitis B virus transactivator X protein is not tumorigenic in transgenic mice.
- Enhancement of Hepatitis B Virus Replication by Its X Protein in Transgenic Mice
- Expression of Hepatitis B Virus X Protein Does Not Alter the Accumulation of Spontaneous Mutations in Transgenic Mice
- Interferon-Regulated Pathways That Control Hepatitis B Virus Replication in Transgenic Mice†
- The hepatitis B virus (HBV) precore protein inhibits HBV replication in transgenic mice.