ArticleJournal of virology2007
Herpes simplex virus latency-associated transcript sequence downstream of the promoter influences type-specific reactivation and viral neurotropism.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 45 citations in OpenAlex.
- Regulatory mimicry of cyclin-dependent kinases by a conserved herpesvirus protein kinase.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Epigenetic Regulation by Polycomb Complexes from Drosophila to Human and Its Relation to Communicable Disease Pathogenesis.International journal of molecular sciences · 2022Review
- Clinical Management of Herpes Simplex Virus Keratitis.Diagnostics (Basel, Switzerland) · 2022Review
- Review
- Local Immune Control of Latent Herpes Simplex Virus Type 1 in Ganglia of Mice and Man.Frontiers in immunology · 2021Review
- Update on Herpes simplex keratitis management.Eye (London, England) · 2020Review
- Herpes Simplex Virus: A Versatile Tool for Insights Into Evolution, Gene Delivery, and Tumor Immunotherapy.Virology : research and treatment · 2020Review
- Herpes Simplex Virus 2 Latency-Associated Transcript (LAT) Region Mutations Do Not Identify a Role for LAT-Associated MicroRNAs in Viral Reactivation in Guinea Pig Genital Models.Journal of virology · 2018Article
- Network analysis of the hominin origin of Herpes Simplex virus 2 from fossil data.Virus evolution · 2017Article
- Stress Hormones Epinephrine and Corticosterone Selectively Modulate Herpes Simplex Virus 1 (HSV-1) and HSV-2 Productive Infections in Adult Sympathetic, but Not Sensory, Neurons.Journal of virology · 2017Article
- Worldwide circulation of HSV-2 × HSV-1 recombinant strains.Scientific reports · 2017Article
- Neurotrophic Factors NGF, GDNF and NTN Selectively Modulate HSV1 and HSV2 Lytic Infection and Reactivation in Primary Adult Sensory and Autonomic Neurons.Pathogens (Basel, Switzerland) · 2017Article
- Herpes Simplex Virus 1 Reactivates from Autonomic Ciliary Ganglia Independently from Sensory Trigeminal Ganglia To Cause Recurrent Ocular Disease.Journal of virology · 2015Article
- Characterization of herpes simplex virus 2 primary microRNA Transcript regulation.Journal of virology · 2015Article
- Strategies in gene therapy for glioblastoma.Cancers · 2013Article
- Different mechanisms regulate productive herpes simplex virus 1 (HSV-1) and HSV-2 infections in adult trigeminal neurons.Journal of virology · 2013Article
- Herpes simplex virus 1 tropism for human sensory ganglion neurons in the severe combined immunodeficiency mouse model of neuropathogenesis.Journal of virology · 2013Article
- Rapid host immune response and viral dynamics in herpes simplex virus-2 infection.Nature medicine · 2013Article
- Herpes simplex epithelial and stromal keratitis: an epidemiologic update.Survey of ophthalmology · 2012Review
- A5-positive primary sensory neurons are nonpermissive for productive infection with herpes simplex virus 1 in vitro.Journal of virology · 2011Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Herpes simplex virus (HSV) establishes latency in sensory nerve ganglia during acute infection and may later periodically reactivate to cause recurrent disease. HSV type 1 (HSV-1) reactivates more efficiently than HSV-2 from trigeminal ganglia while HSV-2 reactivates more efficiently than HSV-1 from lumbosacral dorsal root ganglia (DRG) to cause recurrent orofacial and genital herpes, respectively. In a previous study, a chimeric HSV-2 that expressed the latency-associated transcript (LAT) from HSV-1 reactivated similarly to wild-type HSV-1, suggesting that the LAT influences the type-specific reactivation phenotype of HSV-2. To further define the LAT region essential for type-specific reactivation, we constructed additional chimeric HSV-2 viruses by replacing the HSV-2 LAT promoter (HSV2-LAT-P1) or 2.5 kb of the HSV-2 LAT sequence (HSV2-LAT-S1) with the corresponding regions from HSV-1. HSV2-LAT-S1 was impaired for reactivation in the guinea pig genital model, while its rescuant and HSV2-LAT-P1 reactivated with a wild-type HSV-2 phenotype. Moreover, recurrences of HSV-2-LAT-S1 were frequently fatal, in contrast to the relatively mild recurrences of the other viruses. During recurrences, HSV2-LAT-S1 DNA increased more in the sacral cord compared to its rescuant or HSV-2. Thus, the LAT sequence region, not the LAT promoter region, provides essential elements for type-specific reactivation of HSV-2 and also plays a role in viral neurotropism. HSV-1 DNA, as quantified by real-time PCR, was more abundant in the lumbar spinal cord, while HSV-2 DNA was more abundant in the sacral spinal cord, which may provide insights into the mechanism for type-specific reactivation and different patterns of central nervous system infection of HSV-1 and HSV-2.
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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.