Regulation of Hepatitis C Virus life-cycle by lncRNA HULC: crosstalk with other host factors

Abstract

Hepatitis C virus (HCV) is a positive sense single-stranded RNA virus. It belongs to the family Flaviviridae and the genus hepacivirus. Following the receptor-mediated endocytosis, HCV genome is released into the cytoplasm, where it is first translated in association with ER. The translated viral proteins signal re-distribution of cellular membranes to form a membranous web structure. This membranous structure makes the site of viral replication. This not only acts as a closed site where all the required factors can be ‘concentrated’ to achieve efficient replication, it also helps the virus escape immune surveillance. HCV infected cell is also triggered to synthesize increased amount of lipid. This assists in the efficient assembly and release of HCV particle via VLDL release pathway. Increased lipid synthesis also contributes to HCV-induced hepato-steatosis. Taken together, the study suggests a novel role of HULC in HCV life-cycle. It also uncovers the novel association of HULC and hnRNPC1/C2 and its impact on HCV replication. At this stage it can be considered that HULC acts as a double-edged sword, on one side benefitting the HCV particle release, but on the other exhibiting its antiviral effect