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A conformational change in the Cricket Paralysis Virus IRES upon double translocation in the ribosome uncovers an unexpected similarity with the Hepatitis C Virus IRES.

Shortened hepatitis C therapy, with retreatment if needed, can reduce antiviral drug use in patients with mild liver disease, but day 2 viral load is not an adequate predictor of outcome.

Naïve CD8⁺ T cells are dysregulated during chronic hepatitis C (HCV) infection, and this is reversible after viral clearance.

The crystal structure of neutralizing antibody AR3X in complex with HCV E2 glycoprotein reveals unusual features of antibody recognition in which a conserved epitope is recognized by distinct antibody poses.

A novel and potent receptor-binding-blockage human neutralizing antibody prevents HBV infection, and suppresses HBV infection therapeutically in HBV-infected mice.

Beyond well-recognized individual-level risk factors, HIV and hepatitis C transmission among people who inject drugs are further impacted by social and spatial network composition, and spaces in particular may represent efficient means for disseminating interventions that diffuse through the network.

Duck Hepatitis B core protein forms capsids with a slowly folding extension domain which folding competence is important for viral replication.

Small molecule antivirals that drive assembly of HBV capsid protein can also bind to pre-assembled capsids causing them to change morphology or even break, suggesting a complex transduction of binding effects across the capsid.

The mechanism triggering HBV membrane fusion involves ERp57, a cellular protein disulfide isomerase, and ultimately leads to the exposition of a fusion peptide that was identified in the pre-S1 determinant.

The combination of in vitro investigations, the zebrafish screening model and rodent experiments offered a unique approach to optimizing nanoparticles modified with Hepatitis B virus-derived peptides to specifically target hepatocytes.