Abstract
Infection of AGMK or CV-1 cells by the early simian virus 40 mutant tsA58 at the permissive temperature (32 degrees C) followed by a shift to the nonpermissive temperature (41 degrees C) caused a substantial decrease in the levels of late viral RNA in the cytoplasm of AGMK cells but not CV-1 cells. At the translational level, this depression of late viral RNA levels was reflected by a decrease in late viral protein synthesis. Thus, in AGMK cells, an early region gene product (presumably large T-antigen) appeared to be continuously required for efficient expression of the late viral genes. In contrast, late simian virus 40 gene expression, once it is initiated in CV-1 cells, continued efficiently regardless of the tsA mutation. The difference in expression of the late simian virus 40 genes in these tsA mutant-infected monkey kidney cell lines may reflect a difference in host cell proteins which regulate viral gene expression in conjunction with early viral proteins.
MeSH Terms
Animals
Cell Line
Chlorocebus aethiops
Gene Expression Regulation
Mutation
Protein Biosynthesis
RNA, Messenger/metabolism
RNA, Viral/metabolism
Simian virus 40/genetics
Temperature
Transcription, Genetic
Chemicals
RNA, Messenger
RNA, Viral
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Alwine J C
Khoury G
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