Infection of CV1 cells expressing the polyoma virus middle T antigen or the SV40 agnogene product with simian virus 40 host-range mutants |
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Authors: | Susan L Spence Lois C Tack Jocelyn H Wright Susan Carswell James M Pipas |
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Institution: | (1) Department of Biological Sciences, University of Pittsburgh, 15260 Pittsburgh, Pennsylvania;(2) Molecular Biology and Virology Laboratory, The Salk Institute for Biological Studies, 92138 San Diego, California;(3) Department of Microbiology, University of Pennsylvania School of Medicine, 19104 Philadelphia, Pennsylvania |
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Abstract: | Summary SV40 viruses bearing mutations at the carboxy-terminus of large T antigen exhibit a host-range phenotype: such viruses are
able to grow in BSC monkey kidney cells at 37° C, but give at least 10 000-fold lower yields than wild type virus in BSC cells
at 32° C or in CV1 monkey kidney cells at either temperature. The block to infection in the nonpermissive cell type occurs
after the onset of viral DNA replication. Infectious progeny virions are produced at very low efficiency. Although capsid
proteins are synthesized at decreased levels, this does not account for the magnitude of the defect. Presumably some step
of virion assembly or maturation is affected in these mutants. We have previously reported that the viral agnogene product,
a protein throught to be involved in viral assembly or release, fails to accumulate in CV1 cells infected with host-range
mutants. In polyoma virus the middle T antigen plays a role in virion maturation by influencing the phosphorylation of capsid
proteins. In this communication we show that host-range mutants fail to undergo productive infection of CV1 cells expressing
middle T antigen. These mutants do form plaques on an agnoprotein-expressing cell line. However, the agnoprotein does not
seem to act by correcting the mutational block but rather increases the efficiency of plaque formation.
This work was supported by grants CA40586 and BRSG 2S07RR07084-23 to J. M. P. and grant CA33079 to L. T., from the National
Institutes of Health, Bethesda, MD. |
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Keywords: | SV40 large T antigen host-range mutants agnoprotein polyoma virus middle T antigen |
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