Vicky M.-H. Sung

TL;DR: It is demonstrated that acute and chronic HCV infection caused a 5- to 10-fold increase in mutation frequency in Ig heavy chain, BCL-6, p53, and β-catenin genes of in vitro HCV-infected B cell lines andHCV-associated peripheral blood mononuclear cells, lymphomas, and HCCs.

TL;DR: Detergent-resistant membrane (DRM) fractions containing NS proteins and viral RNA were capable ofHCV RNA synthesis using the endogenous HCV RNA template, and suggested that the HCV RCs are protected within lipid rafts.

TL;DR: It is unequivocally established that HCV infects B cells in vivo and in vitro and shows significantly enhanced apoptosis.

TL;DR: It is reported that HCV infection causes production of reactive oxygen species (ROS) and lowering of mitochondrial transmembrane potential (ΔΨm) in in vitro HCV-infected cell cultures, and ROS, along with the previously identified NO, are identified as the primary inducers of DSBs and mitochondrial damage in HCV -infected cells.

TL;DR: Hepatitis C virus infection directly induces TLR4 expression and thereby activates B cells, which may contribute to the host's innate immune responses, and this study analyzes expression and regulation in human B cells following HCV infection in vitro.