Chao-Kuen Lai

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: It is proposed that microtubules and actin filaments provide the tracks for the movement of HCV RCs to other regions in the cell, and the molecular interactions between RCs and micro Tubules, orRCs and actIn filaments, are mediated by NS3 and NS5A.

TL;DR: It is demonstrated that NS3/4A impairs the efficiency of DNA repair by interacting with ATM and renders the cells more sensitive to DNA damage, which may contribute to HCV oncogenesis.

TL;DR: It is proposed that Anxa2 recruits HCV NS proteins and enriches them on the lipid raft to form the HCV replication complex.

TL;DR: It is demonstrated that the movement of core protein to the early and late endosomes and virus production require an endosome-based secretory pathway, independent of that of the internalization of endocytosed virus particles during virus entry.