δ-Infection and suppression of hepatitis B virus replication in chronic HBsAg carriers

✍ Scribed by Kim Krogsgaard; Peter Kryger; Jan Aldershvile; Poul Andersson; Thorkild I. A. Sørensen; Jens Ole Nielsen

• Publisher: John Wiley and Sons
• Year: 1987
• Tongue: English
• Weight: 436 KB
• Volume: 7
• Category: Article
• ISSN: 0270-9139
• DOI: 10.1002/hep.1840070110

✦ Synopsis

The presence of hepatitis B virus DNA and anti-b was examined in a longitudinal study of 24 patients known to be &infected during the course from acute to chronic hepatitis B virus infection. Fifteen patients (63%) were hepatitis B virus DNA positive in the first serum sample. Eleven of 14 patients, who cleared hepatitis B virus DNA, did 80 following or at the same time as onset of 8infection. Duration of hepatitis B virus DNA positivity in these 11 patients was shorter than in 11 anti-tnegative controls matched according to duration of preceding hepatitis B virus DNA positivity, but the difference was not statistically significant. Considering only patients positive for IgM anti-6 in the last serum sample (eight patients), a statistically significant shorter duration of hepatitis B virus DNA positivity was found in 6infected patients than in the controls (p < 0.02). The study indicates that the 6-agent may have the capacity to inhibit hepatitis B virus replication and that a chronic &infection may lead to a termination of the period of active viral replication.

The &agent is a pseudotype virus consisting of an outer shell of hepatitis B virus (HBV)-derived HBsAg enclosing a nucleoprotein in which the &antigen is complexed with the small 6-RNA genome (1, 2). Depending on this HBV helper function, the &agent can infect either chronic HBsAg carriers or individuals simultaneously infected by HBV (3). Infection by the 6-agent has been shown to influence both acute and chronic HBV infection in an unfavorable way (4-7). For example, 6superinfection in an HBsAg carrier may lead to fulminant hepatitis or rapidly progressive liver disease, and co-infection with HBV and 6-agent seems to increase the risk of fulminant hepatitis (8-10).

Experimental &infection of chronic HBV-infected chimpanzees leads to decreasing levels of HBV gene products (HBsAg and HBcAg) (3). In accordance with