Abstract
The past decade has seen tremendous progress in understanding hepatitis C virus (HCV) biology and its related disease, hepatitis C. Major advances in characterizing viral replication have led to the development of direct-acting anti-viral therapies that have considerably improved patient treatment outcome and can even cure chronic infection. However, the high cost of these treatments, their low barrier to viral resistance, and their inability to prevent HCV-induced liver cancer, along with the absence of an effective HCV vaccine, all underscore the need for continued efforts to understand the biology of this virus. Moreover, beyond informing therapies, enhanced knowledge of HCV biology is itself extremely valuable for understanding the biology of related viruses, such as dengue virus, which is becoming a growing global health concern. Major advances have been realized over the last few years in HCV biology and pathogenesis, such as the discovery of the envelope glycoprotein E2 core structure, the generation of the first mouse model with inheritable susceptibility to HCV, and the characterization of virus-host interactions that regulate viral replication or innate immunity. Here, we review the recent findings that have significantly advanced our understanding of HCV and highlight the major challenges that remain.
Highlights
Hepatitis C virus (HCV) is a single-stranded, positive-sense RNA virus of the Flaviviridae family
Considerable progress has been made to understand HCV biology through the generation of increasingly relevant cell culture systems and animal models. These advances recently reached a milestone by the generation of effective direct-acting anti-viral agents (DAAs)[2] able to cure HCV
Their low barrier to resistance-associated mutations combined with their inability to treat challenging patient groups, HCV-induced liver disease, and hepatocellular carcinoma (HCC) all underscore the need for novel, cost-effective DAAs3–6
Summary
Hepatitis C virus (HCV) is a single-stranded, positive-sense RNA virus of the Flaviviridae family. This structure provides a clearer basis for p7-mediated cation conductance and insights on developing channel activity inhibition strategies Another interesting report demonstrated that HCV’s hijacking of host innate immune signaling pathways enhances viral assembly. Hepatocytes from donors with clinically less favorable IFNλ genotypes were more permissive to HCV infection and exhibited reduced anti-viral responses compared with cells from donors with favorable alleles[81] This represents additional, strong evidence that IFNλ alleles can predict the HCV permissiveness and innate immune responses of a particular host genetic background. One solution lies in the development and production of novel, cost-effective DAAs or antibodies that could cure HCV patients This possibility is supported by data from recent studies that demonstrated that passively administered anti-HCV envelope[92] and anti-CLDN1 antibodies can cure human liver chimeric mice of chronic HCV infection[93]. We apologize to all colleagues whose work could not be cited because of space constraints
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