Abstract:
: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 virion 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 p53KOs 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.
journal_name
Virologyjournal_title
Virologyauthors
Kuan MI,O'Dowd JM,Chughtai K,Hayman I,Brown CJ,Fortunato EAdoi
10.1016/j.virol.2016.07.021subject
Has Abstractpub_date
2016-10-01 00:00:00pages
279-293eissn
0042-6822issn
1096-0341pii
S0042-6822(16)30189-1journal_volume
497pub_type
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