JVI Figure table search 04
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Nogal, M. L.
Right arrow Articles by Revilla, Y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nogal, M. L.
Right arrow Articles by Revilla, Y.

Journal of Virology, March 2001, p. 2535-2543, Vol. 75, No. 6
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.6.2535-2543.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

African Swine Fever Virus IAP Homologue Inhibits Caspase Activation and Promotes Cell Survival in Mammalian Cells

María L. Nogal,1 Gonzalo González de Buitrago,2 Clara Rodríguez,1 Beatriz Cubelos,1 Angel L. Carrascosa,1 María L. Salas,1 and Yolanda Revilla1,*

Centro de Biología Molecular "Severo Ochoa" (C.S.I.C.-U.A.M.)1 and Centro Nacional de Biotecnología (C.S.I.C.),2 Universidad Autónoma de Madrid, 28049 Madrid, Spain

Received 19 October 2000/Accepted 11 December 2000

African swine fever virus (ASFV) A224L is a member of the inhibitor of apoptosis protein (IAP) family. We have investigated the antiapoptotic function of the viral IAP both in stably transfected cells and in ASFV-infected cells. A224L was able to substantially inhibit caspase activity and cell death induced by treatment with tumor necrosis factor alpha and cycloheximide or staurosporine when overexpressed in Vero cells by gene transfection. We have also observed that ASFV infection induces caspase activation and apoptosis in Vero cells. Furthermore, using a deletion mutant of ASFV lacking the A224L gene, we have shown that the viral IAP modulates the proteolytic processing of the effector cell death protease caspase-3 and the apoptosis which are induced in the infected cells. Our findings indicate that A224L interacts with the proteolytic fragment of caspase-3 and inhibits the activity of this protease during ASFV infection. These observations could indicate a conserved mechanism of action for ASFV IAP and other IAP family members to suppress apoptosis.


* Corresponding author. Mailing address: Centro de Biología Molecular "Severo Ochoa" (C.S.I.C.-U.A.M.), Universidad Autónoma, 28049 Madrid, Spain. Phone: 3491-397.84.86. Fax: 3491-397.47.99. E-mail: yrevilla{at}cbm.uam.es.


Journal of Virology, March 2001, p. 2535-2543, Vol. 75, No. 6
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.6.2535-2543.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.



This article has been cited by other articles:




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. Mol. Cell. Biol. Microbiol. Mol. Biol. Rev.
Clin. Vaccine Immunol. ALL ASM JOURNALS

Copyright © 2001 by the American Society for Microbiology. All rights reserved.