The pre-S region determines the intracellular localization and appearance of hepatitis B virus.

TL;DR: The impact of virus-host interactions for the pathogenesis of HBV infection and liver disease are discussed, including the relevance of naturally occurring viral variants for clinical disease, the role of viruses-induced apoptosis for HBV-induced liver cell injury and the impact of antiviral immune responses for outcome of infection.

TL;DR: Experimental data and studies in humans show that several specific mutations in the preS/S gene may induce an imbalance in the synthesis of the surface proteins and their consequent retention within the endoplasmic reticulum of the hepatocytes.

TL;DR: Laser capture microdissection demonstrates that different GGHs may contain specific mutants and exhibit differential biological activities.

TL;DR: Screening of patients with advanced chronic hepatitis B and C with hepatic ultrasound and determination of serum alfa-fetoprotein may improve the detection of HCC, but further studies are needed to determine whether screening improves clinical outcome.

TL;DR: Duck hepatitis B virus, a DNA virus closely related to human hepatitis Birus, was studied in infected duck liver and a pathway for the replication of the DNA genome of hepatitis B-like viruses by reverse transcription of an RNA intermediate is proposed.

TL;DR: In southern Italy, 44 contacts of hepatitis B virus carriers, including infants of carrier mothers, became HBsAg positive despite passive and active immunisation according to standard protocols, and infection was confirmed by the presence of additional markers of viral replication.

TL;DR: Immunological cross-reactions showed that P39/GP42 is partially homologous to P24/GP27 and GP33/GP36, and a model is presented of how the open reading frame for the viral envelope leads to defined amounts of three different proteins.

TL;DR: In vitro infection of uninfected hepatocyte cultures with DHBV demonstrates that a similar 50-fold amplification of CCC DNA occurs during an early stage in the infection before virus production, which may account for the ability of hepadnavirus-infected cells persistently to produce virus particles in the absence of stable integration of viral DNA.