ArticleJCI insight2016
In vivo disruption of latent HSV by designer endonuclease therapy.
Article in JCI insight, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 39 citations in OpenAlex.
- Advances in gene transfer technologies: comparing viral and non-viral vectors for therapeutic applications.3 Biotech · 2026Review
- Epigenetic drugs against human DNA viruses and retroviruses.Antiviral research · 2025Review
- CRISPR/Cas9 Eye Drop HSV-1 Treatment Reduces Brain Viral Load: A Novel Application to Prevent Neuronal Damage.Pathogens (Basel, Switzerland) · 2024Article
- Gene editing for latent herpes simplex virus infection reduces viral load and shedding in vivo.Nature communications · 2024Article
- Summary of the Centers for Disease Control and Prevention/National Institute of Allergy and Infectious Diseases Joint Workshop on Genital Herpes: 3-4 November 2022.Open forum infectious diseases · 2024Review
- Modulation of Equid Herpesvirus-1 Replication DynamicsViruses · 2024Article
- Engineered extracellular vesicles efficiently deliver CRISPR-Cas9 ribonucleoprotein (RNP) to inhibit herpes simplex virus1 infectionActa pharmaceutica Sinica. B · 2024Article
- Liver-Humanized NSG-PiZ Mice Support the Study of Chronic Hepatitis B Virus Infection and Antiviral Therapies.Microbiology spectrum · 2023Article
- Meganuclease targeting HSV-1 protects against herpetic keratitis: Application to corneal transplants.Molecular therapy. Nucleic acids · 2022Article
- Current landscape in antiviral drug development against herpes simplex virus infections.Smart medicine · 2022Review
- Clinical Management of Herpes Simplex Virus Keratitis.Diagnostics (Basel, Switzerland) · 2022Review
- Article
- Improvements of nuclease and nickase gene modification techniques for the treatment of genetic diseases.Frontiers in genome editing · 2022Review
- Chromatin-mediated epigenetic regulation of HSV-1 transcription as a potential target in antiviral therapy.Antiviral research · 2021Review
- Targeting herpes simplex virus with CRISPR-Cas9 cures herpetic stromal keratitis in mice.Nature biotechnology · 2021Article
- Optimization of AAV vectors to target persistent viral reservoirs.Virology journal · 2021Review
- CRISPR-Cas9 gene editing of hepatitis B virus in chronically infected humanized mice.Molecular therapy. Methods & clinical development · 2021Article
- Review
- RNA-guided gene editing of the murine gammaherpesvirus 68 genome reduces infectious virus production.PloS one · 2021Article
- Local Immune Control of Latent Herpes Simplex Virus Type 1 in Ganglia of Mice and Man.Frontiers in immunology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
A large portion of the global population carries latent herpes simplex virus (HSV), which can periodically reactivate, resulting in asymptomatic shedding or formation of ulcerative lesions. Current anti-HSV drugs do not eliminate latent virus from sensory neurons where HSV resides, and therefore do not eliminate the risk of transmission or recurrent disease. Here, we report the ability of HSV-specific endonucleases to induce mutations of essential HSV genes both in cultured neurons and in latently infected mice. In neurons, viral genomes are susceptible to endonuclease-mediated mutagenesis, regardless of the time of treatment after HSV infection, suggesting that both HSV lytic and latent forms can be targeted. Mutagenesis frequency after endonuclease exposure can be increased nearly 2-fold by treatment with a histone deacetylase (HDAC) inhibitor. Using a mouse model of latent HSV infection, we demonstrate that a targeted endonuclease can be delivered to viral latency sites via an adeno-associated virus (AAV) vector, where it is able to induce mutation of latent HSV genomes. These data provide the first proof-of-principle to our knowledge for the use of a targeted endonuclease as an antiviral agent to treat an established latent viral infection in vivo.
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.