ArticleJournal of virology2001
Fate of the inner nuclear membrane protein lamin B receptor and nuclear lamins in herpes simplex virus type 1 infection.
Article in Journal of virology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
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Who cites it
75 citing papers in PubMed, 121 citations in OpenAlex.
- A Comprehensive Review of Nuclear Mechanics: Advances, Disease Relevance, Methodologies, and AI Applications.Cell biochemistry and biophysics · 2026Review
- Primary envelopment of Kaposi's sarcoma-associated herpesvirus at the nucleoplasmic reticulum.Journal of virology · 2025Article
- Mechanisms for assembly of the nucleoplasmic reticulum.Cellular and molecular life sciences : CMLS · 2024Review
- Review
- Three-Dimensional Chromatin Structure of the EBV Genome: A Crucial Factor in Viral Infection.Viruses · 2023Review
- Intranuclear HSV-1 DNA ejection induces major mechanical transformations suggesting mechanoprotection of nucleus integrity.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Nuclear Cytoskeleton in Virus Infection.International journal of molecular sciences · 2022Review
- The Role of Lamins in the Nucleoplasmic Reticulum, a Pleiomorphic Organelle That Enhances Nucleo-Cytoplasmic Interplay.Frontiers in cell and developmental biology · 2022Review
- Herpes Simplex Virus 1 UL34 Mutants That Affect Membrane Budding Regulation and Nuclear Lamina Disruption.Journal of virology · 2021Article
- Mechanism of Nuclear Lamina Disruption and the Role of pUS3 in HSV-1 Nuclear Egress.Journal of virology · 2021Article
- Review
- Characterization of lamin B receptor of Sf9 cells and its fate during Autographa californica nucleopolyhedrovirus infection.Cytotechnology · 2020Article
- Roles of the Interhexamer Contact Site for Hexagonal Lattice Formation of the Herpes Simplex Virus 1 Nuclear Egress Complex in Viral Primary Envelopment and Replication.Journal of virology · 2019Article
- Remodeling of host membranes during herpesvirus assembly and egress.Protein & cell · 2019Review
- A Nondimensional Model Reveals Alterations in Nuclear Mechanics upon Hepatitis C Virus Replication.Biophysical journal · 2019Article
- Nuclear envelope impairment is facilitated by the herpes simplex virus 1 Us3 kinase.F1000Research · 2019Article
- Epstein-Barr Virus-Induced Nodules on Viral Replication Compartments Contain RNA Processing Proteins and a Viral Long Noncoding RNA.Journal of virology · 2018Article
- Three-dimensional imaging reveals endo(sarco)plasmic reticulum-containing invaginations within the nucleoplasm of muscle.American journal of physiology. Cell physiology · 2018Article
- Baculovirus infection induces disruption of the nuclear lamina.Scientific reports · 2017Article
- Article
15 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During herpesvirus egress, capsids bud through the inner nuclear membrane. Underlying this membrane is the nuclear lamina, a meshwork of intermediate filaments with which it is tightly associated. Details of alterations to the lamina and the inner nuclear membrane during infection and the mechanisms involved in capsid transport across these structures remain unclear. Here we describe the fate of key protein components of the nuclear envelope and lamina during herpes simplex virus type 1 (HSV-1) infection. We followed the distribution of the inner nuclear membrane protein lamin B receptor (LBR) and lamins A and B(2) tagged with green fluorescent protein (GFP) in live infected cells. Together with additional results from indirect immunofluorescence, our studies reveal major morphologic distortion of nuclear-rim LBR and lamins A/C, B(1), and B(2). By 8 h p.i., we also observed a significant redistribution of LBR-GFP to the endoplasmic reticulum, where it colocalized with a subpopulation of cytoplasmic glycoprotein B by immunofluorescence. In addition, analysis by fluorescence recovery after photobleaching reveals that LBR-GFP exhibited increased diffusional mobility within the nuclear membrane of infected cells. This is consistent with the disruption of interactions between LBR and the underlying lamina. In addition to studying stably expressed GFP-lamins by fluorescence microscopy, we studied endogenous A- and B-type lamins in infected cells by Western blotting. Both approaches reveal a loss of lamins associated with virus infection. These data indicate major disruption of the nuclear envelope and lamina of HSV-1-infected cells and are consistent with a virus-induced dismantling of the nuclear lamina, possibly in order to gain access to the inner nuclear membrane.
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