Roles for herpes simplex virus type 1 U{sub L}34 and U{sub S}3 proteins in disrupting the nuclear lamina during herpes simplex virus type 1 egress
- Department of Microbiology, The University of Iowa, 3115 Medical Laboratories, Iowa City, IA 52242 (United States)
Cells infected with wild type HSV-1 showed significant lamin A/C and lamin B rearrangement, while U{sub L}34-null virus-infected cells exhibited few changes in lamin localization, indicating that U{sub L}34 is necessary for lamin disruption. During HSV infection, U{sub S}3 limited the development of disruptions in the lamina, since cells infected with a U{sub S}3-null virus developed large perforations in the lamin layer. U{sub S}3 regulation of lamin disruption does not correlate with the induction of apoptosis. Expression of either U{sub L}34 or U{sub S}3 proteins alone disrupted lamin A/C and lamin B localization. Expression of U{sub L}34 and U{sub 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{sub L}34 and U{sub S}3 in regulating the state of the nuclear lamina during viral infection.
- OSTI ID:
- 20779478
- Journal Information:
- Virology, Vol. 347, Issue 2; Other Information: DOI: 10.1016/j.virol.2005.11.053; PII: S0042-6822(05)00800-7; Copyright (c) 2005 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0042-6822
- Country of Publication:
- United States
- Language:
- English
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