Lack of in vivo blockade of Fas- and TNFR1-mediated hepatocyte apoptosis by the hepatitis C virus.
Details
State: Public
Version: author
License: Not specified
Serval ID
serval:BIB_0266FC684B4C
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Lack of in vivo blockade of Fas- and TNFR1-mediated hepatocyte apoptosis by the hepatitis C virus.
Journal
The Journal of pathology
ISSN
0022-3417 (Print)
ISSN-L
0022-3417
Publication state
Published
Issued date
08/2002
Peer-reviewed
Oui
Volume
197
Number
5
Pages
617-623
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Publication Status: ppublish
Abstract
In vitro data have shown that the hepatitis C virus (HCV) core protein binds to protein members of the tumour necrosis factor receptor (TNFR) superfamily. Since this interaction could be relevant to HCV persistence and oncogenesis, this study assessed whether HCV may interfere with the apoptotic cascade in vivo. Apoptosis (by TUNEL) and Fas and TNFR1 expression (by immunohistochemistry) were scored in the liver of 60 chronic hepatitis C patients. Results were compared with the liver disease grading and staging scores and the HCV replication level in serum and liver. Apoptotic hepatocytes were stained in 29 cases. Fas was expressed in 35 cases and TNFR1 in 21, 15 patients (25%) being negative for both receptors. Overall, the numbers of TUNEL-, Fas- and TNFR-positive hepatocytes did not correlate with the extent of intrahepatic CD8+ T-lymphocyte infiltration, the grading and staging of liver disease, or the serum or liver HCV RNA levels. Furthermore, when patients expressing either Fas or TNFR1 were stratified according to serum HCV RNA levels, cases with detectable hepatocyte apoptosis had higher HCV viraemias. In conclusion, an HCV-mediated, in vivo blockade of hepatocyte apoptosis via the Fas- or TNFR1-dependent pathways seems unlikely.
Keywords
Antigens, CD/metabolism, Apoptosis, CD8-Positive T-Lymphocytes/pathology, Genotype, Hepacivirus/genetics, Hepacivirus/isolation & purification, Hepacivirus/physiology, Hepatitis C, Chronic/immunology, Hepatitis C, Chronic/pathology, Hepatocytes/metabolism, Hepatocytes/pathology, Humans, In Situ Nick-End Labeling, Liver/immunology, Liver/virology, RNA, Viral/blood, Receptors, Tumor Necrosis Factor/metabolism, Receptors, Tumor Necrosis Factor, Type I, Virus Replication, fas Receptor/metabolism
Pubmed
Web of science
Create date
11/06/2021 14:06
Last modification date
07/07/2021 7:08