ArticleJournal of virology2026
Article in Journal of virology, 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
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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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0 citing papers in PubMed.
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Authors and funding
7 authors.
Funding
Abstract
Understanding the organization and connectivity of brain circuits has been a major focus of neuroscience for decades, and viral vectors have been commonly utilized to map neural connections in animal models. The alpha-herpesvirus herpes simplex virus 1 (HSV-1) is one of the most studied and genetically modified viruses due to its bidirectional spread capabilities in the nervous system and replication dependency on the viral thymidine kinase (TK) gene in the terminally differentiated neurons. H129, a brain isolate of HSV-1, is the most promising anterograde neurotracer that has been extensively used to map neuronal projections. Replication-deficient monosynaptic H129 vectors (H129-dTK) have been previously developed. In this study, we report the development and characterization of a new H129-dTK recombinant that expresses mNeonGreen along with FlpO recombinase. We investigated the replication and spread properties of this recombinant utilizing compartmentalized primary neuron culture and FlpO/Cre reporter mouse lines. Our findings reveal that the replication, labeling, and spread phenotypes of H129-dTK recombinants strongly depend on the infecting dose of virus. At higher viral doses, H129-dTK exhibits limited replication and anterograde transsynaptic spread without requiring exogenous TK complementation, which can be visualized using Cre/FlpO reporter mice. This controlled replication reduces tissue damage at the injection site while allowing precise labeling of neuronal output projections. Together, these results provide valuable insights into the replication and spread characteristics of replication-deficient H129 recombinants in neurons
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