Published online Mar 28, 2015. doi: 10.3748/wjg.v21.i12.3480
Peer-review started: November 19, 2014
First decision: December 4, 2014
Revised: December 10, 2014
Accepted: February 5, 2015
Article in press: February 5, 2015
Published online: March 28, 2015
Processing time: 131 Days and 11.9 Hours
Hepatitis C virus (HCV)-specific cytotoxic T cell (CTL) response plays a major role in viral control during spontaneous infection resolution. These cells develop an exhausted and pro-apoptotic status during chronic onset, being unable to get rid of HCV. The role of this response in contributing to sustained viral response (SVR) after anti-HCV is controversial. Recent studies show that after successful interferon-based anti-HCV treatment, HCV traces are still detectable and this correlates with a peak of HCV-specific CTL response activation, probably responsible for maintaining SVR by subsequent complete HCV clearing. Moreover, SVR patients’ serum is still able to induce HCV infection in naïve chimpanzees, suggesting that the infection could be under the control of the immune system after a successful treatment, being transmissible in absence of this adaptive response. At least theoretically, treatment-induced viral load decrease could allow an effective HCV-specific CTL response reestablishment. This effect has been recently described with anti-HCV interferon-free regimes, based on direct-acting antivirals. Nevertheless, this is to some extent controversial with interferon-based therapies, due to the detrimental immunoregulatory α-interferon effect on T cells. Moreover, HCV-specific CTL response features during anti-HCV treatment could be a predictive factor of SVR that could have clinical implications in patient management. In this review, the recent knowledge about the role of HCV-specific CTL response in the development of SVR after anti-HCV treatment is discussed.
Core tip: Hepatitis C virus (HCV)-specific cytotoxic T lymphocyte (CTL) response plays an essential role in controlling acute HCV infection but its implication in treatment-induced viral control is controversial. During interferon/ribavirin treatment, HCV traces persist after sustained viral response (SVR) and this correlates with an activated HCV-specific CTL response, suggesting the necessity of this response to obtain an indefinite viral control. Current data propose that viral suppression during interferon/ribavirin treatment and during direct-acting anti-viral regimes could affect HCV-specific CTL restoration. Moreover, the features of this CTL response during treatment could have a predictive value on SVR outcome.