Apoptosis in cultured cells infected with feline calicivirus.
Caliciviruses are important pathogens of man and animals; feline calicivirus (FCV) is responsible for an acute upper respiratory tract disease in cats. To date, little is known about the mechanism of cell damage induced by these viruses. We set out to determine if apoptosis played any role in cell death in FCV infection of cultured cells. We demonstrate that caspase-2, -3, and -7 were activated during FCV infection, as evidenced by pro-form processing and an increase in acetyl-Asp-Glu-Val-Asp-7-amido-4-trifluoromethylcoumarin cleavage activity, as well as cleavage of poly(ADP-ribose)polymerase. Caspase activation coincided with the condensation of chromatin. At about 8 h post infection we also detected cleavage of the FCV capsid protein; this was prevented by caspase inhibitors. Taken together these results suggest that FCV triggers apoptosis within infected cells and that caspases are involved in the cleavage of the capsid protein.
Roberts
Lisa O
LO
School of Biomedical and Life Sciences, University of Surrey, Guildford, GU2 7XH, United Kingdom.
Al-Molawi
Naema
N
Carter
Michael J
MJ
Kass
George E N
GE
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D015415:Biomarkers; D017927:Calicivirus, Feline / Q000472:pathogenicity*; D020169:Caspases / Q000378:metabolism; D002415:Cats; D002460:Cell Line; D002478:Cells, Cultured; D007668:Kidney; D007700:Kinetics
D015415:Biomarkers; D020169:Caspases