Document Detail

Herpes simplex virus blocks Fas-mediated apoptosis independent of viral activation of NF-kappaB in human epithelial HEp-2 cells.
MedLine Citation:
PMID:  17523868     Owner:  NLM     Status:  MEDLINE    
The goal of our study was to characterize the apoptotic response of herpes simplex virus (HSV)-infected, human epithelial HEp-2 cells to extrinsic treatments through the Fas receptor. Initially, we defined the Fas response of these cells. We found the following: (1) Treatment of HEp-2 cells with anti-Fas antibody or Fas ligand (FasL) alone did not induce apoptosis. (2) In addition, these inducers did not activate NF-kappaB in these cells. (3) The addition of cycloheximide (CHX) during these treatments caused a dramatic increase in programmed cell death. (4) HEp-2 cells infected with HSV for 6 h prior to anti-Fas plus CHX treatment were nonapoptotic, and (5) these cells possessed nuclear NFkappaB. (6) HSV blocked anti-Fas or FasL plus CHX-induced apoptosis in HEp-2 cells that stably expressed a dominant-negative form of IkappaBalpha. These results indicate that HSV infection can block the process of Fas-mediated apoptosis through a mechanism that is independent of viral activation of NFkappaB. Our findings help define the molecular mechanisms involved in HSV evasion of the cytokine-driven, innate immune response in human epithelial cells.
Elise R Morton; John A Blaho
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research     Volume:  27     ISSN:  1079-9907     ISO Abbreviation:  J. Interferon Cytokine Res.     Publication Date:  2007 May 
Date Detail:
Created Date:  2007-05-25     Completed Date:  2007-07-17     Revised Date:  2007-12-03    
Medline Journal Info:
Nlm Unique ID:  9507088     Medline TA:  J Interferon Cytokine Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  365-76     Citation Subset:  IM    
Department of Microbiology, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029, USA.
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MeSH Terms
Antigens, CD95 / immunology,  physiology*
Apoptosis / drug effects,  physiology*
Carcinoma, Hepatocellular / pathology
Cell Line, Tumor
Cell Nucleus / metabolism
Cycloheximide / pharmacology
Epithelial Cells / metabolism,  physiology,  virology
Fluorescent Antibody Technique, Indirect
Liver Neoplasms / pathology
Microscopy, Fluorescence
NF-kappa B / metabolism,  physiology*
Protein Synthesis Inhibitors / pharmacology
Simplexvirus / physiology*
Tumor Necrosis Factor-alpha / physiology
Virus Activation*
Grant Support
Reg. No./Substance:
0/Antigens, CD95; 0/NF-kappa B; 0/Protein Synthesis Inhibitors; 0/Tumor Necrosis Factor-alpha; 66-81-9/Cycloheximide

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