ArticleNucleus (Austin, Tex.)
Simian virus 40 induces lamin A/C fluctuations and nuclear envelope deformation during cell entry.
Article in Nucleus (Austin, Tex.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 49 citations in OpenAlex.
- Lamin A/C maintains genome topology and regulates transcriptional programs essential for virus-driven B cell activation.bioRxiv : the preprint server for biology · 2026Article
- Dynamic Post-translational Modifications of Nuclear Lamins in Cellular Function and Pathophysiology.Sub-cellular biochemistry · 2025Review
- Host proteases: key regulators in viral infection and therapeutic targeting.Frontiers in immunology · 2025Review
- Mouse polyomavirus infection induces lamin reorganisation.The FEBS journal · 2024Article
- Lamin B1 curtails early human papillomavirus infection by safeguarding nuclear compartmentalization and autophagic capacity.Cellular and molecular life sciences : CMLS · 2024Article
- Nuclear Cytoskeleton in Virus Infection.International journal of molecular sciences · 2022Review
- Computational analyses reveal spatial relationships between nuclear pore complexes and specific lamins.The Journal of cell biology · 2021Article
- Sending mixed signals: polyomavirus entry and trafficking.Current opinion in virology · 2021Review
- ER functions are exploited by viruses to support distinct stages of their life cycle.Biochemical Society transactions · 2020Review
- Taking the Scenic Route: Polyomaviruses Utilize Multiple Pathways to Reach the Same Destination.Viruses · 2020Review
- Review
- pH stability and disassembly mechanism of wild-type simian virus 40.Soft matter · 2020Article
- SV40 Hijacks Cellular Transport, Membrane Penetration, and Disassembly Machineries to Promote Infection.Viruses · 2019Review
- A Nondimensional Model Reveals Alterations in Nuclear Mechanics upon Hepatitis C Virus Replication.Biophysical journal · 2019Article
- Nuclear lipid droplets derive from a lipoprotein precursor and regulate phosphatidylcholine synthesis.Nature communications · 2019Article
- Dynein Engages and Disassembles Cytosol-Localized Simian Virus 40 To Promote Infection.Journal of virology · 2018Article
- Article
- Viral hijacking of host caspases: an emerging category of pathogen-host interactions.Cell death and differentiation · 2017Review
- Chromatin and lamin A determine two different mechanical response regimes of the cell nucleus.Molecular biology of the cell · 2017Article
- Nuclear Import of Hepatitis B Virus Capsids and Genome.Viruses · 2017Review
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
The canonical gate of viruses and viral genomes into the nucleus in non-dividing cells is the nuclear pore, embedded within the nuclear envelope. However, we found that for SV40, the nuclear envelope poses a major hurdle to infection: FISH analysis revealed that the majority of viral DNA remains trapped in the ER; silencing of Lamin A/C rendered the cells more susceptible to infection; and proliferating cells are more susceptible to infection than quiescent cells. Surprisingly, we observed that following SV40 infection the nuclear envelope, including lamins A/C, B1, B2 and the nuclear pore complex, was dramatically deformed, as seen by immunohistochemistry. The infection induced fluctuations in the level of lamin A/C, dephosphorylation of an unknown epitope and leakage to the cytoplasm just prior to and during nuclear entry. Deformations were transient, and the spherical structure of the nuclear envelope was restored subsequent to nuclear entry. Nuclear envelope deformations and lamin A/C dephosphorylation depended on caspase-6 cleavage of lamin A/C. Notably, we have previously reported that inhibition of caspase-6 abolishes SV40 infection. Taken together the results suggest that alterations of the nuclear lamina, induced by the infecting virus, are involved in the nuclear entry of the SV40 genome. We propose that SV40 utilize this unique, previously unknown mechanism for direct trafficking of its genome from the ER to the nucleus. As SV40 serves as a paradigm for the pathogenic human BK, JC and Merkel cell polyomavirus, this study suggests nuclear entry as a novel drug target for these infections.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.