Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers.

Many mutation analyses of the HBV genome have been performed in the search for new prognostic markers. However, the Kozak sequence preceding precore was covered only infrequently in these analyses. In this study, the HBV core promoter/precore region was sequenced in serum samples from European inactive HBV carriers.

A new approach for therapeutic vaccination against chronic HBV infections.

There are currently about 257 million people suffering from chronic HBV infection worldwide. In many cases, an insufficient Tcell response is causative for establishment of a chronic infection. To ensure a robust cellular immune response and induction of neutralizing antibodies a novel vaccine platform based on modified cell-permeable HBV capsids was utilized.

Formation of semi-enveloped particles as a unique feature of a hepatitis B virus PreS1 deletion mutant.

Background: Naturally occurring variants with deletions or mutations in the C-terminal PreS1 domain from hepatitis B virus (HBV) chronically infected patients have been shown to promote HBsAg retention, inhibit HBsAg secretion and change the extracellular appearance of PreS1-containing HBV particles (filaments and virions).

Aims: To study the impact of N-terminal deletion in preS1 domain on viral secretion and morphogenesis.

Methods: An HBV mutant with 15 amino acids (aa 25-39) deletion in N-terminal preS1 was isolated.

HCV-induced oxidative stress by inhibition of Nrf2 triggers autophagy and favors release of viral particles.

Viruses are known to exploit the autophagic machinery for their own benefit. In case of the hepatitis C virus autophagy is induced. As autophagy serves as a degradation pathway to maintain cellular homeostasis, it is activated in response to cellular stress such as elevated levels of reactive oxygen species (ROS).