ArticleCell research2010
Thyroid hormone controls the gene expression of HSV-1 LAT and ICP0 in neuronal cells.
Article in Cell research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- Article
- Disturbed Yin-Yang balance: stress increases the susceptibility to primary and recurrent infections of herpes simplex virus type 1.Acta pharmaceutica Sinica. B · 2020Review
- Modulation of Voltage-Gated Sodium Channel Activity in Human Dorsal Root Ganglion Neurons by Herpesvirus Quiescent Infection.Journal of virology · 2020Article
- Virus Infections and Host Metabolism-Can We Manage the Interactions?Frontiers in immunology · 2020Review
- Reversing thyroid-hormone-mediated repression of a HSV-1 promoter via computationally guided mutagenesis.Journal of cell science · 2017Article
- Receipt of thyroid hormone deficiency treatment and risk of herpes zoster.International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases · 2017Article
- Overexpression of thyroid hormone receptor β1 altered thyroid hormone-mediated regulation of herpes simplex virus-1 replication in differentiated cells.Journal of neurovirology · 2016Article
- Influence of thyroid hormone disruption on the incidence of shingles.Epidemiology and infection · 2015Article
- Thyroid hormone-dependent epigenetic suppression of herpes simplex virus-1 gene expression and viral replication in differentiated neuroendocrine cells.Journal of the neurological sciences · 2014Article
- A Novel Thyroid Hormone Mediated Regulation of HSV-1 Gene Expression and Replication is Specific to Neuronal Cells and Associated with Disruption of Chromatin Condensation.SOJ pharmacy & pharmaceutical sciences · 2014Article
- Effects of thyroid hormone on HSV-1 gene regulation: implications in the control of viral latency and reactivation.Cell & bioscience · 2011Article
- A Cohort Historical Analysis of the Relationship between Thyroid Hormone Malady and Alpha-Human Herpesvirus Activation.Journal of steroids & hormonal scienceArticle
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Various factors/pathways including hormonal regulation have been suggested to control herpes simplex virus type 1 (HSV-1) latency and reactivation. Our computer analysis identified a DNA repeat containing thyroid hormone-responsive elements (TRE) in the regulatory region of HSV-1 latency-associated transcript (LAT). Thyroid hormone (triiodothyronine, T(3)) functions via its receptor TR (thyroid hormone receptor), a transcription factor. Present study investigated the roles of TR and T(3) in HSV-1 gene expression using cultured neuoroblastoma cell lines. We demonstrated that liganded TR activated LAT transcription, but repressed infected cell protein no. 0 (ICP0) transcription in the presence of LAT TRE. Chromatin immunoprecipitation (ChIP) assays showed that TRs were recruited to LAT TREs independently of T(3) and hyperacetylated H4 was associated with the LAT promoter that was transcriptionally active. In addition, ChIP results showed that the chromatin insulator protein CCCTC-binding factor was enriched at the LAT TREs in the presence of TR and T(3). In addition, the BRG1 chromatin remodeling complex is found to participate in the T(3)/TR-mediated LAT activation since overexpression of BRG1 enhanced the LAT transcription and the dominant-negative mutant K785R abolished the activation. This is the first report revealing that TR elicits epigenetic regulation on HSV-1 ICP0 expression in neuronal cells and could have a role in the complex processes of HSV-1 latency/reactivation.
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