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Significance of host cell kinases in herpes simplex virus type 1 egress and lamin-associated protein disassembly from the nuclear lamina
Journal article   Open access   Peer reviewed

Significance of host cell kinases in herpes simplex virus type 1 egress and lamin-associated protein disassembly from the nuclear lamina

Natalie R Leach and Richard J Roller
Virology (New York, N.Y.), Vol.406(1), pp.127-137
10/10/2010
DOI: 10.1016/j.virol.2010.07.002
PMCID: PMC2948959
PMID: 20674954
url
https://doi.org/10.1016/j.virol.2010.07.002View
Published (Version of record) Open Access

Abstract

The nuclear lamina is thought to be a steric barrier to the herpesvirus capsid. Disruption of the lamina accompanied by phosphorylation of lamina proteins is a conserved feature of herpesvirus infection. In HSV-1-infected cells, protein kinase C (PKC) alpha and delta isoforms are recruited to the nuclear membrane and PKC delta has been implicated in phosphorylation of emerin and lamin B. We tested two critical hypotheses about the mechanism and significance of lamina disruption. First, we show that chemical inhibition of all PKC isoforms reduced viral growth five-fold and inhibited capsid egress from the nucleus. However, specific inhibition of either conventional PKCs or PKC delta does not inhibit viral growth. Second, we show hyperphosphorylation of emerin by viral and cellular kinases is required for its disassociation from the lamina. These data support hypothesis that phosphorylation of lamina components mediates lamina disruption during HSV nuclear egress.
nuclear lamina HSV-1 nuclear egress emerin protein kinase C

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