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
Abstract 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
키워드
Vesicular stomatitis virus (VSV)protein kinase inibitorKT5720cytoskeletalmatrix (M) protein
저자
Young Sook Kim [ Department of Oriental Medical Food and Nutrition, Asia University ]
한국생물공학회 [The Korean Society for Biotechnology and Bioengineering]
설립연도
1984
분야
공학>생물공학
소개
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