Novel nuclear herniations induced by nuclear localization of a viral protein.
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 sigma1s 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.
Hoyt
Cristen C
CC
Department of Neurology (B-182), University of Colorado Health Sciences Center, 4200 E. 9th Avenue, Denver, CO 80262, USA.
Bouchard
Ron J
RJ
Tyler
Kenneth L
KL
D021581:Active Transport, Cell Nucleus; D036022:Capsid Proteins / Q000235:genetics / Q000378:metabolism*; D002467:Cell Nucleus / Q000378:metabolism* / Q000473:pathology*; D006367:HeLa Cells; D006801:Humans; D012089:Mammalian orthoreovirus 3 / Q000472:pathogenicity*; D008969:Molecular Sequence Data; D034881:Nuclear Lamina / Q000473:pathology; D019913:Nuclear Localization Signals; D022022:Nuclear Pore / Q000473:pathology; D017422:Sequence Analysis, DNA; D014162:Transfection
D036022:Capsid Proteins; D019913:Nuclear Localization Signals; C031728:sigma 1 protein, reovirus