ReviewViruses2021
Host and Viral Factors Involved in Nuclear Egress of Herpes Simplex Virus 1.
Review in Viruses, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Cell death network regulation in HSV infection: immune evasion versus host defense.Apoptosis : an international journal on programmed cell death · 2026Review
- Metformin inhibits nuclear egress of chromatin fragments in senescence and aging.Nature aging · 2026Article
- HSV-1 US3: A Master Mimic Hijacking Host Kinase Networks for Viral Dominance.Journal of medical virology · 2025Review
- ER protein CLCC1 promotes nuclear envelope fusion in herpesviral and host processes.Nature communications · 2025Article
- ESCRT-III is recruited by human herpesvirus 6A nuclear egress complex to promote nuclear egress of the nucleocapsid.Journal of virology · 2025Article
- Controlling Much? Viral Control of Host Chromatin Dynamics.Annual review of virology · 2024Review
- 'Getting Better'-Is It a Feasible Strategy of Broad Pan-Antiherpesviral Drug Targeting by Using the Nuclear Egress-Directed Mechanism?International journal of molecular sciences · 2024Review
- Phosphatidic acid signaling and function in nuclei.Progress in lipid research · 2024Review
- Human herpesvirus 6A nuclear matrix protein U37 interacts with heat shock transcription factor 1 and activates the heat shock response.Journal of virology · 2023Article
- HSV-1 exploits host heterochromatin for nuclear egress.The Journal of cell biology · 2023Article
- HSV-1 selectively packs the transcription factor Oct-1 into EVs to facilitate its infection.Frontiers in microbiology · 2023Article
- CD98 heavy chain as a prognostic biomarker and target for cancer treatment.Frontiers in oncology · 2023Review
- Correlative Cryo-imaging Using Soft X-Ray Tomography for the Study of Virus Biology in Cells and Tissues.Sub-cellular biochemistry · 2023Article
- Review
- Review
- Role of the Orphan Transporter SLC35E1 in the Nuclear Egress of Herpes Simplex Virus 1.Journal of virology · 2022Article
- The human cytomegalovirus decathlon: Ten critical replication events provide opportunities for restriction.Frontiers in cell and developmental biology · 2022Review
- Infection-induced chromatin modifications facilitate translocation of herpes simplex virus capsids to the inner nuclear membrane.PLoS pathogens · 2021Article
- Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Herpes simplex virus 1 (HSV-1) replicates its genome and packages it into capsids within the nucleus. HSV-1 has evolved a complex mechanism of nuclear egress whereby nascent capsids bud on the inner nuclear membrane to form perinuclear virions that subsequently fuse with the outer nuclear membrane, releasing capsids into the cytosol. The viral-encoded nuclear egress complex (NEC) plays a crucial role in this vesicle-mediated nucleocytoplasmic transport. Nevertheless, similar system mediates the movement of other cellular macromolecular complexes in normal cells. Therefore, HSV-1 may utilize viral proteins to hijack the cellular machinery in order to facilitate capsid transport. However, little is known about the molecular mechanisms underlying this phenomenon. This review summarizes our current understanding of the cellular and viral factors involved in the nuclear egress of HSV-1 capsids.
Indexed as
Identifiers
What OpenQuestion holds
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.