Published online Oct 14, 2015. doi: 10.3748/wjg.v21.i38.10739
Peer-review started: May 20, 2015
First decision: June 23, 2015
Revised: July 6, 2015
Accepted: September 14, 2015
Article in press: September 14, 2015
Published online: October 14, 2015
Processing time: 148 Days and 21 Hours
The host innate and adaptive immune systems are involved in nearly every step of hepatitis C virus (HCV) infection. In patients, the outcome is determined by a series of complex host-virus interactions, whether it is a natural infection or results from clinical intervention. Strong and persistent CD8+ and CD4+ T-cell responses are critical in HCV clearance, as well as cytokine-induced factors that can directly inhibit virus replication. Newly available direct-acting antivirals (DAAs) are very effective in viral clearance in patients. DAA treatment may further result in the down-regulation of programmed death-1, leading to rapid restoration of HCV-specific CD8+ T cell functions. In this review, we focus on recent studies that address the host responses critical for viral clearance and disease resolution. Additional discussion is devoted to the prophylactic vaccine development as well as to current efforts aimed at understanding the host innate responses against HCV infection. Current theories on how the ubiquitin system and interferon-stimulated genes may affect HCV replication are also discussed.
Core tip: Hepatitis C virus (HCV) is an etiologic agent that can cause severe liver diseases, including chronic hepatitis, liver fibrosis, liver cirrhosis, and hepatocellular carcinoma. Although newly available direct-acting antivirals (DAAs) are very effective in viral clearance in patients, it remains unclear as to how many of the world’s infected individuals will benefit from the new DAAs. In this review, we focus on recent studies that address the host responses critical for viral clearance and disease resolution. Additional discussion is devoted to the prophylactic vaccine development and innate responses against HCV infection. Current theories on how the ubiquitin system and interferon-stimulated genes may affect HCV replication are also discussed.