Journal
VIROLOGY
Volume 497, Issue -, Pages 279-293Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2016.07.021
Keywords
p53; Human Cytomegalovirus; Capsids; Nuclear egress; Infoldings of the inner nuclear membrane (IINM); Secondary envelopment; Transmission electron microscopy (TEM)
Categories
Funding
- NIH [RO1 AI051563]
- COBRE program [P20 RR015587]
- INBRE program [P20 GM103408]
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Human Cytomegalovirus (HCMV) infection is compromised in cells lacking p53, a transcription factor that mediates cellular stress responses. In this study we have investigated compromised functional vision production in cells with p53 knocked out (p53KOs). Infectious center assays found most p53KOs released functional virions. Analysis of electron micrographs revealed modestly decreased capsid production in infected p53KOs compared to wt. Substantially fewer p53KO5 displayed HCMV-induced infoldings of the inner nuclear membrane (IINMs). In p53KOs, fewer capsids were found in IINMs and in the cytoplasm. The deficit in virus-induced membrane remodeling within the nucleus of p53KOs was mirrored in the cytoplasm, with a disproportionately smaller number of capsids re-enveloped. Reintroduction of p53 substantially recovered these deficits. Overall, the absence of p53 contributed to inhibition of the formation and function of IINMs and re-envelopment of the reduced number of capsids able to reach the cytoplasm. (C) 2016 Elsevier Inc. All rights reserved.
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