NDLI: Activation of extrinsic apoptosis pathway in HCV monoinfected and HIV–HCV coinfected patients, irrespective of liver disease severity

Content Provider	Springer Nature Link
Author	Feuth, Thijs Baarle, Debbie Hoepelman, Andy I. M. Erpecum, Karel J. Siersema, Peter D. Arends, Joop E.
Copyright Year	2014
Abstract	Chronic hepatitis C virus (HCV) infection is associated with increased levels of peripheral T cell apoptosis. We aimed to study whether T cell apoptosis markers indicate pathways that may contribute to clinical progression in HCV monoinfected and HIV–HCV coinfected patients. Activation of the extrinsic apoptosis pathways was measured by levels of death receptor Fas, initiator caspase 8 and effector caspases 3 and 7 activity and Annexin V binding on peripheral CD4 and CD8 T cells of HCV monoinfected and HIV/HCV coinfected patients, as well as healthy controls and HIV-infected, hepatitis B virus-infected and primary biliary cirrhosis disease controls. Association with liver fibrosis was assessed by biopsy or by transient elastography. HCV monoinfected and HIV–HCV coinfected patients displayed enhanced peripheral CD4 and CD8 T cell apoptosis. Caspase 8 activity was highest in HIV–HCV coinfection, without enhanced downstream activity of caspases 3 and 7. Level of peripheral T cell apoptosis was independent of liver fibrosis or other disease parameters in all disease groups. The extrinsic apoptosis pathway is upregulated in HCV monoinfection and HIV–HCV coinfection, but this is independent of liver disease severity.
Starting Page	1128
Ending Page	1135
Page Count	8
File Format	PDF
ISSN	13608185
Journal	Apoptosis
Volume Number	19
Issue Number	7
e-ISSN	1573675X
Language	English
Publisher	Springer US
Publisher Date	2014-04-22
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Apoptosis T lymphocytes Liver fibrosis HCV HIV Cancer Research Cell Biology Oncology Biochemistry Virology
Content Type	Text
Resource Type	Article
Subject	Pharmaceutical Science Biochemistry (medical) Cell Biology Clinical Biochemistry Cancer Research Pharmacology

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