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J Virol, August 1998, p. 6699-6709, Vol. 72, No. 8
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Viral Ribonucleoprotein Complex Formation and Nucleolar-Cytoplasmic Relocalization of Nucleolin in Poliovirus-Infected Cells

Shelly Waggonerdagger and Peter Sarnow*

Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California 94305, and Department of Biochemistry, Biophysics and Genetics, University of Colorado Health Sciences Center, Denver, Colorado 80262

Received 2 February 1998/Accepted 15 April 1998

The poliovirus 3' noncoding region (3'NCR) is involved in the efficient synthesis of viral negative-stranded RNA molecules. A strong interaction between a 105-kDa host protein and the wild-type 3'NCR, but not with a replication-defective mutant 3'NCR, was detected. This 105-kDa protein was identified as nucleolin which predominantly resides in the nucleolus and has been proposed to function in the folding of rRNA precursor molecules. A functional role for nucleolin in viral genome amplification was examined in a cell-free extract which has been shown to support the assembly of infectious virus from virion RNA. At early times of viral gene expression, extracts depleted of nucleolin produced less infectious virus than extracts depleted of fibrillarin, another resident of the nucleolus, indicating a functional role of nucleolin in the early stages of the viral life cycle in this in vitro system. Immunofluorescence analysis of uninfected and infected cells showed a nucleocytoplasmic relocalization of nucleolin, but not of fibrillarin, in poliovirus-infected cells. Relocalization of nucleolin was not simply a consequence of virally induced inhibition of translation or transcription, because inhibitors of translation or transcription did not induce nucleolar-cytoplasmic relocalization of nucleolin. These findings suggest a novel virus-induced mechanism by which certain nucleolar proteins are selectively redistributed in infected cells.

* Corresponding author. Present address: Department of Microbiology and Immunology, Fairchild Science Building, Stanford University School of Medicine, Stanford, CA 94305. Phone: (650) 498-7076. Fax: (650) 498-7147. E-mail: psarnow{at}leland.stanford.edu.

dagger Present address: Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305.

J Virol, August 1998, p. 6699-6709, Vol. 72, No. 8
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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