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

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.

Exploiting virus-encoded ion channels as drug targets drove a multi-faceted approach to deriving potent small molecules targeting HCV p7, simultaneously providing new insights into its fundamental biology.

Integrated analysis of IFN-λ and HCV amino acid variation indicates the key role of host innate immunity in viral control.

Incompatibilities between the viral replication machinery and orthologs of the essential host factor cyclophilin A (CypA) contribute to the narrow host range of hepatitis C virus.

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

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.

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.

Interactions between viral genomes within the same cells can impact the selection of drug-resistant variants and this has been finessed by hepatitis C virus.

Very frequent viral kinetics in liver transplant patients reveals that the liver is not only the source of hepatitis C virus (HCV) production, but also plays a major role in extracellular HCV clearance.