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Dev Biol Stand. 1998;94:191-205.

Host range analysis of simian virus 40, BK virus and chimaeric SV40/BKV: relative expression of large T-antigen and Vp1 in infected and transformed cells.

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  • 1Department of Veterans Affairs Medical Center, Research Service, Geriatric Research Education and Clinical Center, Salt Lake City, Utah 84148, USA.

Abstract

Simian virus 40 (SV40) persists in Rhesus monkeys and productively infects cultured simian kidney cells. In contrast to the closely related human virus BKV, SV40 is known to propagate inefficiently in human embryonic kidney (HEK) cells and human fibroblasts (HFF). We examined the growth of SV40, BKV and the chimaeric genome virus, SV40/RFV, in several types of human cells. We analysed replication, expression of T-Ag and Vp1 capsid proteins, and cytopathic effects (CPE). We also compared T-Ag and Vp1 expression in infected versus transformed HFF cells. Although SV40 DNA replicated in HFF and in one subtype of HEK cells, viral DNA accumulated slowly and did not reach high levels until six to eight weeks after transfection. In HFF or HEK cells there was little T-Ag produced but Vp1 was produced in significant amounts in HFF cells. In HFF cells the Vp1/T-Ag ratio was approximately 200: 1, and expression of the viral late region appeared to inhibit expression of the T-Ag gene. In contrast, BKV and the SV40/RFV hybrid propagated well in HEK and HFF cells. The Vp1/T-Ag ratios were also high in BKV and SV40/RFV infected HFF cells but more T-Ag was produced with BKV and SV40/RFV Because SV40/RFV contained the RFV capsid genes but a SV40 T-Ag gene and regulatory region, the human versus simian host range of SV40 was controlled by the viral late region, or one or more capsid proteins. This suggested that the production of small amounts of T-Ag could not by itself account for poor growth of SV40 in HFF cells and that very small, barely detectable amounts of T-Ag were sufficient to activate Vp1 gene expression. Also, although some feature of the SV40 late region prevented rapid growth of the virus in HFF cells, poor virus growth could not be explained by the inability to produce a significant amount of Vp1. Although little T-Ag accumulated in SV40 infected HFF and HEK cells, transformants contained large amounts of T-Ag. In transformants there was a reversal of the Vp1/T-Ag ratio, such that T-Ag was now in 10-20 fold greater amount than Vp1. The relatively large amount of T-Ag in transformants could be accounted for by the relative absence of Vp1, which may inhibit T-Ag production, or by integration of the T-Ag gene at a site in the cell DNA which allows for elevated T-Ag gene expression.

PMID:
9776240
[PubMed - indexed for MEDLINE]
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