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Journal of Virology, June 2004, p. 6360-6369, Vol. 78, No. 12
0022-538X/04/$08.00+0 DOI: 10.1128/JVI.78.12.6360-6369.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
Departments of Immunology,1 Microbiology,6 Neurology,3 Medicine,4 Program in Neurosciences, University of Colorado Health Sciences Center,5 Denver Veterans Affairs Medical Center, Denver, Colorado 802622
Received 15 December 2003/ Accepted 5 February 2004
A common consequence of viral infection is perturbation of host cell nuclear functions. For cytoplasmically replicating viruses, this process may require regulated transport of specific viral proteins into the nucleus. Here, we describe a novel form of virus-induced perturbation of host cell nuclear structures. Active signal-mediated nuclear import of the reovirus
1s protein results in redistribution of nuclear pore complexes and nuclear lamins and formation of nuclear herniations. These herniations represent a previously undescribed mechanism by which cytoplasmic viral infection can perturb nuclear architecture and induce cytopathic effects, which ultimately lead to disease pathogenesis in the infected host.
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