ArticleMolecular cell2014
Co-opting the Fanconi anemia genomic stability pathway enables herpesvirus DNA synthesis and productive growth.
Article in Molecular cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- The Host Cell Factor Phosphatase-2A Subunit PR130 Restricts Replication of Herpes Simplex Virus Type-1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The FANCD2-FANCI heterodimer coordinates chromatin openness and cell cycle progression throughout DNA double-strand break repair.Cell reports · 2026Article
- Human cytomegalovirus regulates host DNA repair machinery for viral genome integrity.Nucleic acids research · 2026Article
- Review
- HIV-1 exploits the Fanconi anemia pathway for viral DNA integration.Cell reports · 2022Article
- Review
- Suppression of non-homologous end joining does not rescue DNA repair defects in Fanconi anemia patient cells.Cell cycle (Georgetown, Tex.) · 2020Article
- TOP2β-Dependent Nuclear DNA Damage Shapes Extracellular Growth Factor Responses via Dynamic AKT Phosphorylation to Control Virus Latency.Molecular cell · 2019Article
- The Exonuclease Activity of Herpes Simplex Virus 1 UL12 Is Required for Production of Viral DNA That Can Be Packaged To Produce Infectious Virus.Journal of virology · 2017Article
- Article
- Human Papillomavirus and the DNA Damage Response: Exploiting Host Repair Pathways for Viral Replication.Viruses · 2017Review
- The herpes simplex virus 1 UL36USP deubiquitinase suppresses DNA repair in host cells via deubiquitination of proliferating cell nuclear antigen.The Journal of biological chemistry · 2017Article
- Host cell restriction factors that limit transcription and replication of human papillomavirus.Virus research · 2017Review
- Article
- Herpes Simplex Virus Latency: The DNA Repair-Centered Pathway.Advances in virology · 2017Review
- Review
- Selective recruitment of host factors by HSV-1 replication centers.Dong wu xue yan jiu = Zoological research · 2015Article
- HSV-I and the cellular DNA damage response.Future virology · 2015Article
- NEDDylation is essential for Kaposi's sarcoma-associated herpesvirus latency and lytic reactivation and represents a novel anti-KSHV target.PLoS pathogens · 2015Article
- The Transcription and Translation Landscapes during Human Cytomegalovirus Infection Reveal Novel Host-Pathogen Interactions.PLoS pathogens · 2015Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
DNA damage associated with viral DNA synthesis can result in double-strand breaks that threaten genome integrity and must be repaired. Here, we establish that the cellular Fanconi anemia (FA) genomic stability pathway is exploited by herpes simplex virus 1 (HSV-1) to promote viral DNA synthesis and enable its productive growth. Potent FA pathway activation in HSV-1-infected cells resulted in monoubiquitination of FA effector proteins FANCI and FANCD2 (FANCI-D2) and required the viral DNA polymerase. FANCD2 relocalized to viral replication compartments, and FANCI-D2 interacted with a multisubunit complex containing the virus-encoded single-stranded DNA-binding protein ICP8. Significantly, whereas HSV-1 productive growth was impaired in monoubiquitination-defective FA cells, this restriction was partially surmounted by antagonizing the DNA-dependent protein kinase (DNA-PK), a critical enzyme required for nonhomologous end-joining (NHEJ). This identifies the FA-pathway as a cellular factor required for herpesvirus productive growth and suggests that FA-mediated suppression of NHEJ is a fundamental step in the viral life cycle.
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Registered trials
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.