J Gen Virol Email Content Delivery
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Gen Virol 87 (2006), 357-361; DOI 10.1099/vir.0.81399-0

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
Right arrow Citation Map
Services
Right arrow Email this article to a friend
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 arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Natoni, A.
Right arrow Articles by Roberts, L. O.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Natoni, A.
Right arrow Articles by Roberts, L. O.
Agricola
Right arrow Articles by Natoni, A.
Right arrow Articles by Roberts, L. O.
© 2006 Society for General Microbiology

Short Communication

The mitochondrial pathway of apoptosis is triggered during feline calicivirus infection

Alessandro Natoni, George E. N. Kass, Michael J. Carter and Lisa O. Roberts

School of Biomedical and Molecular Sciences, University of Surrey, Guildford, Surrey GU2 7XH, UK

Correspondence
Lisa O. Roberts
l.roberts{at}surrey.ac.uk

Feline calicivirus (FCV) belongs to the family Caliciviridae and is an important pathogen of the upper respiratory tract of cats. Recent studies have shown that cells infected with FCV undergo apoptosis, as evidenced by caspase activation, chromatin condensation and cleavage of poly(ADP-ribose) polymerase. Here, the upstream events were investigated in order to define the molecular mechanism of apoptosis in FCV-infected cells. It was shown that FCV induced translocation of phosphatidylserine to the cell outer membrane and release of cytochrome c from mitochondria at about 6–8 h post-infection. These events were preceded by the loss of mitochondrial membrane potential and Bax translocation from the cytosol to mitochondria between 4 and 6 h after infection. Release of cytochrome c from mitochondria triggered the activation of caspase-9 and the subsequent activation of the executioner caspase, caspase-3. These results suggest that the mitochondrial pathway of apoptosis is triggered during FCV infection.




This article has been cited by other articles:


Home page
J. Virol.Home page
K. Bok, V. G. Prikhodko, K. Y. Green, and S. V. Sosnovtsev
Apoptosis in Murine Norovirus-Infected RAW264.7 Cells Is Associated with Downregulation of Survivin
J. Virol., April 15, 2009; 83(8): 3647 - 3656.
[Abstract] [Full Text] [PDF]


Home page
J. Virol.Home page
S. Martin-Latil, L. Mousson, A. Autret, F. Colbere-Garapin, and B. Blondel
Bax Is Activated during Rotavirus-Induced Apoptosis through the Mitochondrial Pathway
J. Virol., May 1, 2007; 81(9): 4457 - 4464.
[Abstract] [Full Text] [PDF]


Home page
J. Gen. Virol.Home page
R. J. Ossiboff, A. Sheh, J. Shotton, P. A. Pesavento, and J. S. L. Parker
Feline caliciviruses (FCVs) isolated from cats with virulent systemic disease possess in vitro phenotypes distinct from those of other FCV isolates
J. Gen. Virol., February 1, 2007; 88(2): 506 - 517.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
INT J SYST EVOL MICROBIOL MICROBIOLOGY J GEN VIROL
J MED MICROBIOL ALL SGM JOURNALS
Copyright © 2006 by the Society for General Microbiology.