Acute Hepatitis A Infection in Hepatitis B Chimpanzee Carriers

✍ Scribed by Kwesi N. Tsiquaye; Tim J. Harrison; Bernard Portmann; Shanlian Hu; Arie J. Zuckerman

• Book ID: 102849213
• Publisher: John Wiley and Sons
• Year: 1984
• Tongue: English
• Weight: 769 KB
• Volume: 4
• Category: Article
• ISSN: 0270-9139
• DOI: 10.1002/hep.1840040325

✦ Synopsis

Two hepatitis B virus carrier chimpanzees which were superinfected with hepatitis A virus developed acute hepatitis followed by the production of antibodies to hepatitis A virus. The Southern blot technique employed to monitor liver hepatitis B virus DNA revealed that the amount of viral DNA in both animals was significantly reduced during the acute phase of hepatitis A infection. The levels of plasma hepatitis B DNA polymerase activity were also reduced in one chimpanzee. The high titers of HBsAg in the circulation remained unchanged throughout the study, and antibodies to the surface antigen and to e antigen were not detected. The morphological lesions in the liver were severe in one chimpanzee from whom one specimen showed both periportal focal necrosis and zonal parenchymal necrosis.

Hepatitis A is a self-limiting disease with long-lasting immunity. However, infection with hepatitis B virus (HBV) may result, in a proportion of patients, in latent infection following integration of HBV DNA in the liver without expression of HBsAg or in persistent infection with expression of HBsAg or the virus (the carrier state). Survival of HBV is ensured by a huge reservoir of carriers estimated to number 200 million worldwide (1). Although the course and duration of the carrier state are unpredictable, spontaneous loss of HBsAg in HBV carriers and seroconversion occur, albeit with low frequency, at periods varying from 18 to 73 months after documented acute hepatitis B infection (2-4). The underlying mechanism of spontaneous clearance of the viral antigens and seroconversion is unknown. However, infection with hepatitis A virus (HAV) (5, 6) or with the 6 agent (7) superimposed upon persistent HBV infection have resulted in the loss of HBsAg with formation of surface antibody (anti-HBs).