Feline calicivirus replication induces apoptosis in cultured cells.
Infection of Crandell-Rees feline kidney (CRFK) cells by feline calicivirus (FCV) causes rapid cytopathic effects followed by cell death. In this study, we observed that FCV replication in cells results in the induction of changes characteristic of apoptosis, including translocation of phosphatidyl serine to the cell outer membrane, chromatin condensation, and oligonucleosomal DNA fragmentation. FCV infection was associated with increases in the activities of caspase-3, -8, and -9, with the level of activation of caspase-3 higher than those of caspases-8 and -9. Caspase activation in CRFK cells was not observed when cells were inoculated with UV-inactivated FCV or when cycloheximide was present during virus infection, indicating that FCV replication and de novo synthesis of virus proteins are critical for induction of apoptosis.
Sosnovtsev
Stanislav V
SV
Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 50 South Drive MSC8007, Building 50, Room 6316, Bethesda, MD 20892-8007, USA. ss216m@nih.gov
Prikhod'ko
Elena A
EA
Belliot
Gaël
G
Cohen
Jeffrey I
JI
Green
Kim Y
KY
D000818:Animals; D017209:Apoptosis; D017927:Calicivirus, Feline / Q000502:physiology*; D020169:Caspases / Q000378:metabolism; D002415:Cats; D002460:Cell Line; D003124:Colorimetry; D004789:Enzyme Activation; D014764:Viral Proteins / Q000096:biosynthesis / Q000502:physiology; D014779:Virus Replication
D014764:Viral Proteins; D020169:Caspases