T-Cell Immunity against the Hepatitis C Virus: A Persistent Research Priority in an Era of Highly Effective Therapy

2020 ◽  
Vol 11 (1) ◽  
pp. a036954 ◽  
Author(s):  
Stephanie Smith ◽  
Jonathan R. Honegger ◽  
Christopher Walker
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
T Cell ◽  
Effective Therapy ◽  
T Cell Immunity ◽  
Research Priority ◽  
Cell Immunity ◽  
Highly Effective

Role of T cell immunity in hepatitis C virus infections

2013 ◽  
Vol 3 (4) ◽  
pp. 461-467 ◽  
Author(s):  
Mark AA Claassen ◽  
Harry LA Janssen ◽  
André Boonstra
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
T Cell ◽  
T Cell Immunity ◽  
Virus Infections ◽  
Cell Immunity

scholarly journals Rapid early innate control of hepatitis C virus during IFN ‐α treatment compromises adaptive CD 4 + T ‐cell immunity

2012 ◽  
Vol 42 (9) ◽  
pp. 2383-2394 ◽  
Author(s):  
Tom Pembroke ◽  
Ian Rees ◽  
Kathleen Gallagher ◽  
Emma Jones ◽  
Paul Mizen ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
T Cell ◽  
T Cell Immunity ◽  
Cell Immunity

T cell immunity in hepatitis B and hepatitis C virus infection: implications for autoimmunity

2005 ◽  
Vol 4 (2) ◽  
pp. 82-95 ◽  
Author(s):  
Yasunori Ichiki ◽  
Xiao-Song He ◽  
Shinji Shimoda ◽  
Hiromi Ishibashi ◽  
Emmet B. Keeffe ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
T Cell ◽  
Virus Infection ◽  
Hepatitis B ◽  
T Cell Immunity ◽  
Hepatitis C Virus Infection ◽  
Cell Immunity

scholarly journals T-cell immunity and hepatitis C virus reinfection after cure of chronic hepatitis C with an interferon-free antiviral regimen in a chimpanzee

Hepatology ◽  
2014 ◽  
Vol 60 (5) ◽  
pp. 1531-1540 ◽  
Author(s):  
Benoit Callendret ◽  
Heather B. Eccleston ◽  
Shelby Hall ◽  
William Satterfield ◽  
Stefania Capone ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
T Cell ◽  
Chronic Hepatitis C ◽  
T Cell Immunity ◽  
Cell Immunity

O.013 Potent T-cell immunity induced by a hepatitis C virus candidate vaccine based on a non-replicative poxvirus

2006 ◽  
Vol 36 ◽  
pp. S4
Author(s):  
G.J. Inchauspe ◽  
A. Fournillier ◽  
E. Gerossier ◽  
A. Evlachev ◽  
P. Martin ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
T Cell ◽  
T Cell Immunity ◽  
Candidate Vaccine ◽  
Cell Immunity

scholarly journals Hepatitis C virus adaptations to altered CD8+ T-cell immunity during pregnancy

2014 ◽  
Vol 9 (4) ◽  
pp. 333-336 ◽  
Author(s):  
Aryn A Price ◽  
Arash Grakoui ◽  
Jonathan R Honegger
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
T Cell ◽  
Cd8 T Cell ◽  
T Cell Immunity ◽  
Cell Immunity

scholarly journals Influence of IFNL3 and HLA-DPB1 genotype on postpartum control of hepatitis C virus replication and T-cell recovery

2016 ◽  
Vol 113 (38) ◽  
pp. 10684-10689 ◽  
Author(s):  
Jonathan R. Honegger ◽  
Dana Tedesco ◽  
Jennifer A. Kohout ◽  
Mona R. Prasad ◽  
Aryn A. Price ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
T Cell ◽  
Virus Replication ◽  
Multivariable Analysis ◽  
Hcv Infection ◽  
T Cell Immunity ◽  
Cell Recovery ◽  
Viral Control ◽  
Cell Immunity

Chronic hepatitis C virus (HCV) infection is characterized by exhaustion of virus-specific T-cells and stable viremia. Pregnancy is an exception. Viremia gradually climbs during gestation but sometimes declines sharply in the months following delivery. Here, we demonstrated that postpartum HCV control was associated with enhanced virus-specific T-cell immunity. Women with viral load declines of at least 1 log10 between the third trimester and 3-mo postpartum exhibited HCV-specific T-cell responses of greater breadth (P = 0.0052) and magnitude (P = 0.026) at 3-mo postpartum than women who failed to control viremia. Moreover, viral dynamics were consistent in women after consecutive pregnancies, suggesting genetic underpinnings. We therefore searched for genetic associations with human leukocyte antigen (HLA) alleles and IFN-λ3 gene (IFNL3) polymorphisms that influence HCV infection outcome. Postpartum viral control was associated with the IFNL3 rs12979860 genotype CC (P = 0.045 at 6 mo) that predicts a positive response to IFN-based therapy. Suppression of virus replication after pregnancy was also strongly influenced by the HLA class II DPB1 locus. HLA-DPB1 alleles are classified by high and low patterns of expression. Carriage of at least one high-expression HLA-DPB1 allele predicted resurgent virus-specific T-cell immunity and viral control at 3-mo postpartum (P = 0.0002). When considered together in multivariable analysis, IFNL3 and HLA-DPB1 independently affected viral control at 3- and 6-mo postpartum. Together, these findings support a model where spontaneous control of HCV such as sometimes follows pregnancy is governed by genetic polymorphisms that affect type III IFN signaling and virus-specific cellular immune responses.

scholarly journals Anti-Hepatitis C Virus T-Cell Immunity in the Context of Multiple Exposures to the Virus

PLoS ONE ◽  
2015 ◽  
Vol 10 (6) ◽  
pp. e0130420 ◽  
Author(s):  
Katja Pfafferott ◽  
Pooja Deshpande ◽  
Elizabeth McKinnon ◽  
Shahzma Merani ◽  
Andrew Lucas ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
T Cell ◽  
T Cell Immunity ◽  
Multiple Exposures ◽  
Cell Immunity

scholarly journals Abnormal Priming of CD4+ T Cells by Dendritic Cells Expressing Hepatitis C Virus Core and E1 Proteins

2002 ◽  
Vol 76 (10) ◽  
pp. 5062-5070 ◽  
Author(s):  
Pablo Sarobe ◽  
Juan José Lasarte ◽  
Noelia Casares ◽  
Ascensión López-Díaz de Cerio ◽  
Elena Baixeras ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
T Cell ◽  
Interleukin 2 ◽  
T Cell Immunity ◽  
Cell Immunity ◽  
Chronic Hcv ◽  
Antigen Presenting

ABSTRACT Patients infected with hepatitis C virus (HCV) have an impaired response against HCV antigens while keeping immune competence for other antigens. We hypothesized that expression of HCV proteins in infected dendritic cells (DC) might impair their antigen-presenting function, leading to a defective anti-HCV T-cell immunity. To test this hypothesis, DC from normal donors were transduced with an adenovirus coding for HCV core and E1 proteins and these cells (DC-CE1) were used to stimulate T lymphocytes. DC-CE1 were poor stimulators of allogeneic reactions and of autologous primary and secondary proliferative responses. Autologous T cells stimulated with DC-CE1 exhibited a pattern of incomplete activation characterized by enhanced CD25 expression but reduced interleukin 2 production. The same pattern of incomplete lymphocyte activation was observed in CD4+ T cells responding to HCV core in patients with chronic HCV infection. However, CD4+ response to HCV core was normal in patients who cleared HCV after alpha interferon therapy. Moreover, a normal CD4+ response to tetanus toxoid was found in both chronic HCV carriers and patients who had eliminated the infection. Our results suggest that expression of HCV structural antigens in infected DC disturbs their antigen-presenting function, leading to incomplete activation of anti-HCV-specific T cells and chronicity of infection. However, presentation of unrelated antigens by noninfected DC would allow normal T-cell immunity to other pathogens.

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