ArticlePLoS pathogens2021
Infection-induced chromatin modifications facilitate translocation of herpes simplex virus capsids to the inner nuclear membrane.
Article in PLoS pathogens, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Nucleus softens during herpesvirus infection.PLoS pathogens · 2026Article
- Polyclonal LC3B Antibodies Generate Non-Specific Staining in the Nucleus of Herpes Simplex Virus Type 1-Infected Cells: Caution in the Interpretation of LC3 Staining in the Immunofluorescence Analysis of Viral Infections.International journal of molecular sciences · 2025Article
- Herpes simplex virus type 1 reshapes host chromatin architecture via transcription machinery hijacking.Nature communications · 2025Article
- Herpes simplex virus assembly and spread in murine skin after infection from the outside.Journal of virology · 2025Article
- Controlling Much? Viral Control of Host Chromatin Dynamics.Annual review of virology · 2024Review
- A deep learning method that identifies cellular heterogeneity using nanoscale nuclear features.Nature machine intelligence · 2024Article
- HSV-1 exploits host heterochromatin for nuclear egress.The Journal of cell biology · 2023Article
- Redundant and Specific Roles of A-Type Lamins and Lamin B Receptor in Herpes Simplex Virus 1 Infection.Journal of virology · 2022Article
- Nuclear speckles - a driving force in gene expression.Journal of cell science · 2022Review
- G2/M checkpoint regulation and apoptosis facilitate the nuclear egress of parvoviral capsids.Frontiers in cell and developmental biology · 2022Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Herpes simplex virus capsids are assembled and packaged in the nucleus and move by diffusion through the nucleoplasm to the nuclear envelope for egress. Analyzing their motion provides conclusions not only on capsid transport but also on the properties of the nuclear environment during infection. We utilized live-cell imaging and single-particle tracking to characterize capsid motion relative to the host chromatin. The data indicate that as the chromatin was marginalized toward the nuclear envelope it presented a restrictive barrier to the capsids. However, later in infection this barrier became more permissive and the probability of capsids to enter the chromatin increased. Thus, although chromatin marginalization initially restricted capsid transport to the nuclear envelope, a structural reorganization of the chromatin counteracted that to promote capsid transport later. Analyses of capsid motion revealed that it was subdiffusive, and that the diffusion coefficients were lower in the chromatin than in regions lacking chromatin. In addition, the diffusion coefficient in both regions increased during infection. Throughout the infection, the capsids were never enriched at the nuclear envelope, which suggests that instead of nuclear export the transport through the chromatin is the rate-limiting step for the nuclear egress of capsids. This provides motivation for further studies by validating the importance of intranuclear transport to the life cycle of HSV-1.
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