Holly L. Hanson

TL;DR: Incomplete control of HCV replication by memory CD8+ Tcells in the absence of adequate CD4+ Tcell help was associated with emergence of viral escape mutations in class I major histocompatibility complex–restricted epitopes and failure to resolve HCV infection.

TL;DR: It is found that in chronic HCV infection, peripheral HCV-specific T cells express high levels ofPD-1 and that blockade of the PD-1/PD-L1 interaction led to an enhanced proliferative capacity.

TL;DR: This study highlights the importance of cytokine deprivation-mediated apoptosis with consequent down-modulation of the immune response to HCV during acute and chronic infections.

TL;DR: Assessment of the effect of each mutation observed during in vivo infection on viral fitness and T cell responses and a recently developed in vitro infectious virus cell culture model suggest that HCV escape mutants emerging early in infection are not necessarily stable, but are eventually replaced with variants that achieve a balance between immune evasion and fitness for replication.

TL;DR: The development of innovative treatment alternatives for HCV-infected patients has been impeded by the lack of in vitro and in vivo systems suitable for the study of HCV infection, replication, and pathogenesis.