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Enhanced duck hepatitis B virus gene expression following aflatoxin B1 exposure.

Publication ,  Journal Article
Barraud, L; Guerret, S; Chevallier, M; Borel, C; Jamard, C; Trepo, C; Wild, CP; Cova, L
Published in: Hepatology
April 1999

Epidemiological studies have suggested synergistic interactions between chronic hepatitis B virus (HBV) infection and aflatoxin B1 (AFB1) exposure in the etiology of hepatocellular carcinoma (HCC), although the molecular mechanisms of their interactions are still not understood. The aim of this study was to use the Pekin duck model to investigate the impact of AFB1 exposure on duck hepatitis B virus (DHBV) replication during the early stages of virus-carcinogen interactions. Six-week-old chronic DHBV-carrier or uninfected ducks were exposed to AFB1 for 5 weeks or treated with dimethylsulfoxide (DMSO) as a control. Animals were observed for 6 to 13 weeks after AFB1 treatment to study the influence of AFB1 exposure on DHBV replication and liver pathologies. Histological analysis showed more marked changes in the livers of AFB1-treated ducks, and these were enhanced by DHBV infection. A significant increase in serum and liver DHBV DNA level was observed in AFB1-treated ducks as compared with DMSO-treated controls. In addition, viral RNAs, in particular the pregenomic RNA that is the template of viral replication, and intrahepatic DHBV DNA replicative intermediates, were significantly increased by AFB1 treatment. Moreover, an overexpression and accumulation of DHBV large envelope (L) protein was observed in the hepatocytes of AFB1-exposed animals. The in vitro study has further confirmed an increase in intracellular viral DNA and in virus release in AFB1-treated primary duck hepatocytes. Taken together, our results indicate that AFB1 exposure leads to an increase in virus gene expression associated with intrahepatic accumulation of DHBV L protein and enhanced liver pathology.

Duke Scholars

Published In

Hepatology

DOI

ISSN

0270-9139

Publication Date

April 1999

Volume

29

Issue

4

Start / End Page

1317 / 1323

Location

United States

Related Subject Headings

  • Virus Replication
  • Viral Envelope Proteins
  • RNA, Viral
  • Male
  • Liver
  • Hepatitis B Virus, Duck
  • Gene Expression Regulation, Viral
  • Gastroenterology & Hepatology
  • Ducks
  • Dose-Response Relationship, Drug
 

Citation

APA
Chicago
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MLA
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Barraud, L., Guerret, S., Chevallier, M., Borel, C., Jamard, C., Trepo, C., … Cova, L. (1999). Enhanced duck hepatitis B virus gene expression following aflatoxin B1 exposure. Hepatology, 29(4), 1317–1323. https://doi.org/10.1002/hep.510290441
Barraud, L., S. Guerret, M. Chevallier, C. Borel, C. Jamard, C. Trepo, C. P. Wild, and L. Cova. “Enhanced duck hepatitis B virus gene expression following aflatoxin B1 exposure.Hepatology 29, no. 4 (April 1999): 1317–23. https://doi.org/10.1002/hep.510290441.
Barraud L, Guerret S, Chevallier M, Borel C, Jamard C, Trepo C, et al. Enhanced duck hepatitis B virus gene expression following aflatoxin B1 exposure. Hepatology. 1999 Apr;29(4):1317–23.
Barraud, L., et al. “Enhanced duck hepatitis B virus gene expression following aflatoxin B1 exposure.Hepatology, vol. 29, no. 4, Apr. 1999, pp. 1317–23. Pubmed, doi:10.1002/hep.510290441.
Barraud L, Guerret S, Chevallier M, Borel C, Jamard C, Trepo C, Wild CP, Cova L. Enhanced duck hepatitis B virus gene expression following aflatoxin B1 exposure. Hepatology. 1999 Apr;29(4):1317–1323.
Journal cover image

Published In

Hepatology

DOI

ISSN

0270-9139

Publication Date

April 1999

Volume

29

Issue

4

Start / End Page

1317 / 1323

Location

United States

Related Subject Headings

  • Virus Replication
  • Viral Envelope Proteins
  • RNA, Viral
  • Male
  • Liver
  • Hepatitis B Virus, Duck
  • Gene Expression Regulation, Viral
  • Gastroenterology & Hepatology
  • Ducks
  • Dose-Response Relationship, Drug