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Caspase-dependent apoptosis in fulminant hepatic failure induced by herpes simplex virus in mice.

Abstract：

BACKGROUND/AIMS:Herpes simplex virus (HSV) is known to induce fulminant hepatic failure. The aim of this study is to clarify the molecular basis of liver injury in HSV-induced hepatitis. METHODS:Immunocompetent mice were inoculated with HSV or ultraviolet-inactivated HSV (UV-HSV) intravenously. Extent of liver injury was evaluated by changes of serum enzymes and histopathology. Apoptosis was assessed by DNA fragmentation and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL). Immunohistochemistry for caspase-3 and Fas ligand was performed. Reverse transcriptase-polymerase chain reaction for Fas ligand was also performed. RESULTS:All mice died of rapid and massive liver cell death after HSV infection, whereas no change was observed in mice after UV-HSV inoculation. The extent of viral replication and DNA fragmentation correlated well with the severity of liver injury. Caspase-3 was activated in the liver after HSV infection, but not UV-HSV. Positive reaction for TUNEL was observed not only in HSV-antigen positive cells but also in HSV-antigen negative cells. Fas ligand was induced in the liver infected with HSV, but not with UV-HSV. CONCLUSIONS:Caspase-dependent apoptosis is involved in HSV-associated liver injury. Not only viral replication but also non-viral factor such as Fas ligand may facilitate rapid development of this disease.

journal_name

J Hepatol

journal_title

Journal of hepatology

authors

Hashimoto K,Minagawa H,Yanagi Y

doi

10.1016/s0168-8278(03)00385-4

subject

Has Abstract

pub_date

2003-11-01 00:00:00

pages

773-8

issue

5

eissn

0168-8278

issn

1600-0641

pii

S0168827803003854

journal_volume

39

pub_type

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