원문정보
초록
영어
The antiviral mechanism of KT5720 is known to inhibit the cAMP-dependent protein kinase (PKA), on the VSV infection in BHK-21cell cultures. The virus inducted CPE (cell rounding) was almost completely suppressed by KT5720 at 5 uM. The inhibitor, however, did not affect the replication of the virus and the synthesis of viral macromolecules. Immunological studies
showed the viral matrix (M) protein displayed intimate association with the cytoskeletal components and probably the cell rounding. KT5720, did not block the cytoskeletal disruption, while the cell rounding was suppressed. These observations suggest that the interaction between the viral M protein and the cytoskeletal components may not be enough to cause the
morphological change of the cell. And, the KT5720-sensitive function may be involved in developing the VSV-induced CPE, but not essential for the virus replications.
목차
INTRODUCTION
MATERIALS AND METHODS
Viruses, cell culture and infectivity assay
Metabolic labeling of viral proteins with radioactiveprecursor
Immunoblot analysis
Antisera
Immunofluorescence studies
Immunoprecipitation
Chemicals and buffers
RESULTS
Effect of K-252a derivatives on the VSV infection inculture
Studies on the effect of KT5720 on the viral proteinsynthesis
Studied on the distribution of viral antigens in thecell
Effects of KT5720 on the cytoskelatal structures
DISCUSSION
REFERENCES