ArticleJournal of virology2010
A double mutation in glycoprotein gB compensates for ineffective gD-dependent initiation of herpes simplex virus type 1 infection.
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed, 59 citations in OpenAlex.
- Syncytium-forming HSV-1 in cancer gene therapy: From molecular mechanisms to clinical translation.Virulence · 2026Review
- Engineering HSV-1 for oncolytic therapy: From molecular entry mechanisms to retargeting strategies.Genes & diseases · 2026Review
- Genetic mutations in HSV-1 replication-defective vectors: Implications for their safety in gene therapy applications.Gene therapy · 2025Article
- Retargeted oncolytic viruses engineered to remodel the tumor microenvironment for glioblastoma immunotherapy.Nature cancer · 2025Article
- An oncolytic herpes simplex virus armed with IL-12 for treatment of preclinical glioblastoma.Molecular therapy. Oncology · 2025Article
- Durable tissue-specific transgene expression in newborn mice following intraperitoneal delivery of non-cytotoxic HSV vectors.Molecular therapy. Methods & clinical development · 2025Article
- Induction of necroptosis in multinucleated giant cells induced by conditionally replicating syncytial oHSV in co-cultures of cancer cells and non-cancerous cells.Molecular therapy. Oncology · 2024Article
- Seek and destroy: Development of novel viral therapy for EGFR-expressing tumors.Molecular therapy. Oncology · 2024Article
- Oncolytic herpes simplex viruses designed for targeted treatment of EGFR-bearing tumors.Molecular therapy. Oncology · 2024Article
- Novel mutations in UMolecular therapy. Methods & clinical development · 2023Article
- Nanobody-based retargeting of an oncolytic herpesvirus for eliminating CXCR4Molecular therapy oncolytics · 2022Article
- Potent anti-tumor effects of receptor-retargeted syncytial oncolytic herpes simplex virus.Molecular therapy oncolytics · 2021Article
- Treatment of glioblastoma with current oHSV variants reveals differences in efficacy and immune cell recruitment.Molecular therapy oncolytics · 2021Article
- Immunomodulatory Arming Factors-The Current Paradigm for Oncolytic Vectors Relies on Immune Stimulating Molecules.International journal of molecular sciences · 2021Review
- Antibody Screening System Using a Herpes Simplex Virus (HSV)-Based Probe To Identify a Novel Target for Receptor-Retargeted Oncolytic HSVs.Journal of virology · 2021Article
- Entry of Alphaherpesviruses.Current issues in molecular biology · 2021Review
- Generation of an Oncolytic Herpes Simplex Viral Vector Completely Retargeted to the GDNF Receptor GFRα1 for Specific Infection of Breast Cancer Cells.International journal of molecular sciences · 2020Article
- Herpes Simplex Virus Oncolytic Immunovirotherapy: The Blossoming Branch of Multimodal Therapy.International journal of molecular sciences · 2020Review
- Design of an Interferon-Resistant Oncolytic HSV-1 Incorporating Redundant Safety Modalities for Improved Tolerability.Molecular therapy oncolytics · 2020Article
- Point Mutations in Retargeted gD Eliminate the Sensitivity of EGFR/EGFRvIII-Targeted HSV to Key Neutralizing Antibodies.Molecular therapy. Methods & clinical development · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Herpes simplex virus (HSV) entry into cells is triggered by the binding of envelope glycoprotein D (gD) to a specific receptor, such as nectin-1 or herpesvirus entry mediator (HVEM), resulting in activation of the fusion effectors gB and gH and virus penetration. Here we report the identification of a hyperactive gB allele, D285N/A549T, selected by repeat passage of a gD mutant virus defective for nectin-1 binding through cells that express a gD-binding-impaired mutant nectin-1. The gB allele in a wild-type virus background enabled the use of other nectins as virus entry receptors. In addition, combination of the mutant allele with an epidermal growth factor receptor (EGFR)-retargeted gD gene yielded dramatically increased EGFR-specific virus entry compared to retargeted virus carrying wild-type gB. Entry of the gB mutant virus into nectin-1-bearing cells was markedly accelerated compared to that of wild-type virus, suggesting that the gB mutations affect a rate-limiting step in entry. Our observations indicate that ineffective gD activation can be complemented by hypersensitization of a downstream component of the entry cascade to gD signaling.
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.