ReviewGenes & diseases2026
Engineering HSV-1 for oncolytic therapy: From molecular entry mechanisms to retargeting strategies.
Review in Genes & diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oncolytic viruses (OVs) represent a cutting-edge approach to cancer immunotherapy, characterized by their ability to selectively infect and eliminate tumor cells while sparing healthy tissues. Among the diverse OVs, type 1 herpes simplex virus (HSV-1) stands out due to its robust oncolytic activity, genetic malleability, broad cell tropism, and well-documented clinical safety. Advances in genetic engineering have further amplified the therapeutic efficacy of HSV-1 by enhancing tumor specificity, replication efficiency, and immunogenicity. Clinically significant HSV-1-based oncolytic viruses, such as T-VEC and G47Δ, have gained regulatory approvals for treating melanoma and malignant glioma, respectively, highlighting their transformative potential in cancer therapy. The attenuation strategies employed in most oncolytic HSV-1 (oHSV-1) strains, while ensuring safety, often reduce viral replication and cytotoxicity. To address this limitation, retargeting strategies focusing on HSV-1 glycoproteins (gD, gH/gL, and gB) have been developed. These modifications aim to abolish canonical receptor interactions and achieve tumor-specific targeting through ligand-receptor binding. Recent breakthroughs in understanding HSV entry mechanisms have enabled the creation of fully retargeted HSV vectors with enhanced specificity and efficacy. This review explores the molecular mechanisms underlying HSV glycoprotein-mediated cell entry, examines recent advances in receptor-retargeted oHSV-1 engineering, and discusses the challenges and future directions in the development of oncolytic HSV-based therapies.
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.