Roles for herpes simplex virus type 1 U(L)34 and U(S)3 proteins in disrupting the nuclear lamina during herpes simplex virus type 1 egress

摘要

Cells infected with wild type HSV-1 showed significant lamin A/C and lamin B rearrangement, while U(L)34-null virus-infected cells exhibited few changes in lamin localization, indicatine that U(L)34 is necessary for lamin disruption. During HSV infection, U(S)3 limited the development of disruptions in the lamina, since cells infected with a U(S)3-null virus developed large perforations in the lamin layer. U(S)3 regulation of lamin disruption does not correlate with the induction of apoptosis. Expression of either U(L)34 or U(S)3 proteins alone disrupted lamin A/C and larnin B localization. Expression of U(L)34 and U(S)3 together had little effect on lamin A/C localization, suggesting a regulatory interaction between the two proteins. The data presented in this paper argue for crucial roles for both U(L)34 and U(S)3 in regulating the state of the nuclear lamina during viral infection. (c) 2005 Elsevier Inc. All rights reserved.