scholarly journals No evidence for abnormal immune activation in peripheral blood T cells in patients with hepatitis C virus (HCV) infection with or without cryoglobulinaemia

1998 ◽  
Vol 113 (1) ◽  
pp. 48-54 ◽  
Author(s):  
P. Cacoub ◽  
L. Musset ◽  
P. Hausfater ◽  
P. Ghillani ◽  
F. L. Fabiani ◽  
...  
Keyword(s):  
T Cells ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Immune Activation ◽  
Peripheral Blood ◽  
Hcv Infection

scholarly journals Kinetic Analysis by Real-Time PCR of Hepatitis C Virus (HCV)-Specific T Cells in Peripheral Blood and Liver after Challenge with HCV

2008 ◽  
Vol 82 (21) ◽  
pp. 10487-10492 ◽  
Author(s):  
Ramesh K. Ramalingam ◽  
Dirk Meyer-Olson ◽  
Naglaa H. Shoukry ◽  
David G. Bowen ◽  
Christopher M. Walker ◽  
...  
Keyword(s):  
T Cells ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
T Cell ◽  
Real Time ◽  
Real Time Pcr ◽  
Peripheral Blood ◽  
Hcv Infection ◽  
Virus Challenge ◽  
Rapid Kinetics

ABSTRACT Intrahepatic virus-specific CD8+ T cells are thought to be important for the control of hepatitis C virus (HCV) infection, yet the precise kinetics for the expansion of epitope-specific T cells over the course of infection are difficult to determine with currently available methods. We used a real-time PCR assay to measure the frequency of clonotypic HCV-specific CD8+ T cells in peripheral blood and snap-frozen liver biopsy specimens of two chimpanzees (Pan troglodytes) with previously resolved HCV infection who were rechallenged with HCV. In response to rechallenge, the magnitude of each clonotypic response was 10-fold higher in the liver than in the blood, and the peak clonotype frequency was concurrent with the peak viral load. The higher frequency of HCV-specific clonotypes in the liver than in peripheral blood was maintained for at least 3 months after the clearance of viremia. After antibody-mediated CD8+ T-cell depletion and another viral challenge, the rebound of these clonotypes was seen prior to an appreciable reconstitution of CD8+ T-cell values and, again, at higher frequencies in the liver than in peripheral blood. These data demonstrate the importance of intrahepatic virus-specific CD8+ T cells for the clearance of infection and the rapid kinetics of expansion after virus challenge.

scholarly journals Quantitative analysis of hepatitis C virus-specific CD8+ T cells in peripheral blood and liver using peptide-MHC tetramers

1999 ◽  
Vol 96 (10) ◽  
pp. 5692-5697 ◽  
Author(s):  
X.-S. He ◽  
B. Rehermann ◽  
F. X. Lopez-Labrador ◽  
J. Boisvert ◽  
R. Cheung ◽  
...  
Keyword(s):  
T Cells ◽  
Hepatitis C Virus ◽  
Quantitative Analysis ◽  
Hepatitis C ◽  
Cd8 T Cells ◽  
Peripheral Blood ◽  
Mhc Tetramers

scholarly journals High Level of PD-1 Expression on Hepatitis C Virus (HCV)-Specific CD8+ and CD4+ T Cells during Acute HCV Infection, Irrespective of Clinical Outcome

2011 ◽  
Vol 85 (9) ◽  
pp. 4633-4633
Author(s):  
V. Kasprowicz ◽  
J. S. zur Wiesch ◽  
T. Kuntzen ◽  
B. E. Nolan ◽  
S. Longworth ◽  
...  
Keyword(s):  
T Cells ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Clinical Outcome ◽  
Cd4 T Cells ◽  
Hcv Infection ◽  
Acute Hcv ◽  
High Level ◽  
Acute Hcv Infection

scholarly journals Differential Effects of Hepatitis C Virus JFH1 on Human Myeloid and Plasmacytoid Dendritic Cells

2009 ◽  
Vol 83 (11) ◽  
pp. 5693-5707 ◽  
Author(s):  
Hua Liang ◽  
Rodney S. Russell ◽  
Nicole L. Yonkers ◽  
David McDonald ◽  
Benigno Rodriguez ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Cd4 T Cells ◽  
Ex Vivo ◽  
Hcv Infection ◽  
Poly I:C ◽  
Dc Function ◽  
Cd40 Expression

ABSTRACT Dendritic cells (DCs) are reported to be functionally deficient during chronic hepatitis C virus (HCV) infection. Differing results have been reported on direct effects of intact replicative-form HCV on DC function. To better understand the effect of HCV on DC function, we treated freshly purified human myeloid DCs (mDCs) and plasmacytoid DCs (pDCs) with HCV JFH1. We found that HCV upregulated mDC maturation marker (CD83, CD86, and CD40) expression and did not inhibit Toll-like receptor 3 (TLR3) ligand [poly(I:C)]-induced mDC maturation, a finding consistent with the phenotype of DCs from HCV-infected subjects. At the same time, HCV JFH1 inhibited the ability of poly(I:C)-treated mDCs to activate naive CD4 T cells. In contrast, although there was no direct effect of virus on pDC maturation, HCV JFH1 inhibited TLR7 ligand (R848)-induced pDC CD40 expression, and this was associated with impaired ability to activate naive CD4 T cells. Parallel experiments with recombinant HCV proteins indicated HCV core protein may be responsible for a portion of the activity. Furthermore, HCV-mediated mDC maturation was dependent upon CD81-E2 interaction and, in part, TLR2. Using UV-treated HCV, we show that HCV-mediated mDC and pDC maturation is virus replication independent and, using strand specific PCR, we found no evidence for HCV replication within DCs. Because these effects of HCV on DC subset maturation and function in part recapitulate direct ex vivo analysis of DCs in chronic HCV infection, the mechanisms described here likely account for a portion of the DC subset defects observed in vivo.

Hepatitis C virus (HCV)-specific CD8+ T cells in patients with recurrent HCV-infection after liver transplantation (OLTx)

2001 ◽  
Vol 34 ◽  
pp. 115
Author(s):  
C.A. Schirren ◽  
N.H. Gruener ◽  
M.C. Jung ◽  
R. Zachoval ◽  
J.T. Gerlach ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
T Cells ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Cd8 T Cells ◽  
Hcv Infection

scholarly journals Impaired Hepatitis C Virus (HCV)-Specific Effector CD8+ T Cells Undergo Massive Apoptosis in the Peripheral Blood during Acute HCV Infection and in the Liver during the Chronic Phase of Infection

2008 ◽  
Vol 82 (20) ◽  
pp. 9808-9822 ◽  
Author(s):  
Henry Radziewicz ◽  
Chris C. Ibegbu ◽  
Huiming Hon ◽  
Melissa K. Osborn ◽  
Kamil Obideen ◽  
...  
Keyword(s):  
T Cells ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
T Cell ◽  
Chronic Phase ◽  
T Cell Response ◽  
Hcv Infection ◽  
Caspase 9 ◽  
Acute Hcv ◽  
Acute Hcv Infection

ABSTRACT A majority of patients infected with hepatitis C virus (HCV) do not sustain an effective T-cell response, and viremia persists. The mechanism leading to failure of the HCV-specific CD8+ T-cell response in patients developing chronic infection is unclear. We investigated apoptosis susceptibility of HCV-specific CD8+ T cells during the acute and chronic stages of infection. Although HCV-specific CD8+ T cells in the blood during the acute phase of infection and in the liver during the chronic phase were highly activated and expressed an effector phenotype, the majority was undergoing apoptosis. In contrast, peripheral blood HCV-specific CD8+ T cells during the chronic phase expressed a resting memory phenotype. Apoptosis susceptibility of HCV-specific CD8+ T cells was associated with very high levels of programmed death-1 (PD-1) and low CD127 expression and with significant functional T-cell deficits. Further evaluation of the “death phase” of HCV-specific CD8+ T cells during acute HCV infection showed that the majority of cells were dying by a process of cytokine withdrawal, mediated by activated caspase 9. Contraction during the acute phase occurred rapidly via this process despite the persistence of the virus. Remarkably, in the chronic phase of HCV infection, at the site of infection in the liver, a substantial frequency of caspase 9-mediated T-cell death was also present. This study highlights the importance of cytokine deprivation-mediated apoptosis with consequent down-modulation of the immune response to HCV during acute and chronic infections.

scholarly journals Hepatitis C Virus as a Unique Human Model Disease to Define Differences in the Transcriptional Landscape of T Cells in Acute versus Chronic Infection

Viruses ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 683 ◽  
Author(s):  
David Wolski ◽  
Georg M. Lauer
Keyword(s):  
T Cells ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Cell Differentiation ◽  
T Cell ◽  
Cd8 T Cells ◽  
T Cell Differentiation ◽  
Hcv Infection ◽  
Early Gene ◽  
Human Model

The hepatitis C virus is unique among chronic viral infections in that an acute outcome with complete viral elimination is observed in a minority of infected patients. This unique feature allows direct comparison of successful immune responses with those that fail in the setting of the same human infection. Here we review how this scenario can be used to achieve better understanding of transcriptional regulation of T-cell differentiation. Specifically, we discuss results from a study comparing transcriptional profiles of hepatitis C virus (HCV)-specific CD8 T-cells during early HCV infection between patients that do and do not control and eliminate HCV. Identification of early gene expression differences in key T-cell differentiation molecules as well as clearly distinct transcriptional networks related to cell metabolism and nucleosomal regulation reveal novel insights into the development of exhausted and memory T-cells. With additional transcriptional studies of HCV-specific CD4 and CD8 T-cells in different stages of infection currently underway, we expect HCV infection to become a valuable model disease to study human immunity to viruses.

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