Herpes simplex virus (HSV)
Herpes Virus Family

Author: Gianpiero Pescarmona
Date: 25/05/2009

Description

DEFINITION

Herpes simplex virus 1 and 2 (HSV-1 and HSV-2) are two strains of the herpesvirus family, Herpesviridae, which cause infections in humans. HSV-1 and 2 are also referred to as Human Herpes Virus 1 and 2 (HHV-1 and HHV-2).

DatabaseLink
Wikipedia"URL":
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EPIDEMIOLOGY

age, sex, seasonality, etc

SYMPTOMS

DIAGNOSIS

histopathology
radiology
NMR
laboratory tests

PATHOGENESIS

PATIENT RISK FACTORS

Iron availability

Genetic

Haptoglobin phenotype

Acquired

Vascular

Genetic

Acquired

Hormonal

Regulation of herpes simplex virus type 1 thymidine kinase gene expression by thyroid hormone receptor in cultured neuronal cells. 2010
J Neurovirol. 2010 Feb;16(1):13-24
Hsia SC, Pinnoji RC, Bedadala GR, Hill JM, Palem JR.

Department of Basic Pharmaceutical Sciences, University of Louisiana at Monroe College of Pharmacy, Monroe, LA 71209, USA. hsia@ulm.edu

Herpes simplex virus type 1 (HSV-1) undergoes acute infection in epithelial cells followed by establishment of latency in the neurons of trigeminal ganglia. The latent virus maintains a dormant state and can recurs spontaneously, suggesting transcriptional silencing and reactivation occur in neurons. Computer data mining identified a nuclear hormone response element (NRE), the binding site for the thyroid hormone receptor (TR) or other nuclear hormone receptor, in the promoter of HSV-1 thymidine kinase (TK). TRs are transcription factors whose activity is dependent on their ligand thyroid hormone (T(3); triiodothyronine). We hypothesize that TR and T(3) exert regulation on HSV-1 gene expression in neurons. A neuroblastoma cell line expressing the TR isoform beta (N2aTRbeta) was utilized for in vitro investigation. Results showed that liganded TR repressed TK promoter activity but unliganded TR relieved the inhibition. The mutagenesis study demonstrated that one nucleotide mutation at the NRE abolished the T(3)/TR-mediated regulation. N2aTRbeta cells treated with T(3) were suppressive to TK expression and virus release but the removal of T(3) de-repressed TK expression and increased virus release, confirmed by reverse transcriptase-polymerase chain reaction (RT-PCR) and plaque assays, respectively. Chromatin immunoprecipitation (ChIP) assays showed that TRs were enriched at TK NRE in the presence of T(3). Additional results demonstrated that hyper acetylated histone H4 and monomethylated H3 modified at lysine 9 (H3K9me1) were enriched at transcriptionally active TK promoters but were dissociated from the NRE by T(3)/TR. These results suggest that T(3) could regulate HSV-1 gene expression through its receptor via histone modification in cultured neuronal cells.

Genetic

Acquired

TISSUE SPECIFIC RISK FACTORS

anatomical (due its structure)

vascular (due to the local circulation)

physiopathological (due to tissue function and activity)

COMPLICATIONS

THERAPY

Regulation of herpes simplex virus type 1 thymidine kinase gene expression by thyroid hormone receptor in cultured neuronal cells. 2010
J Neurovirol. 2010 Feb;16(1):13-24
Hsia SC, Pinnoji RC, Bedadala GR, Hill JM, Palem JR.

Department of Basic Pharmaceutical Sciences, University of Louisiana at Monroe College of Pharmacy, Monroe, LA 71209, USA. hsia@ulm.edu

Herpes simplex virus type 1 (HSV-1) undergoes acute infection in epithelial cells followed by establishment of latency in the neurons of trigeminal ganglia. The latent virus maintains a dormant state and can recurs spontaneously, suggesting transcriptional silencing and reactivation occur in neurons. Computer data mining identified a nuclear hormone response element (NRE), the binding site for the thyroid hormone receptor (TR) or other nuclear hormone receptor, in the promoter of HSV-1 thymidine kinase (TK). TRs are transcription factors whose activity is dependent on their ligand thyroid hormone (T(3); triiodothyronine). We hypothesize that TR and T(3) exert regulation on HSV-1 gene expression in neurons. A neuroblastoma cell line expressing the TR isoform beta (N2aTRbeta) was utilized for in vitro investigation. Results showed that liganded TR repressed TK promoter activity but unliganded TR relieved the inhibition. The mutagenesis study demonstrated that one nucleotide mutation at the NRE abolished the T(3)/TR-mediated regulation. N2aTRbeta cells treated with T(3) were suppressive to TK expression and virus release but the removal of T(3) de-repressed TK expression and increased virus release, confirmed by reverse transcriptase-polymerase chain reaction (RT-PCR) and plaque assays, respectively. Chromatin immunoprecipitation (ChIP) assays showed that TRs were enriched at TK NRE in the presence of T(3). Additional results demonstrated that hyper acetylated histone H4 and monomethylated H3 modified at lysine 9 (H3K9me1) were enriched at transcriptionally active TK promoters but were dissociated from the NRE by T(3)/TR. These results suggest that T(3) could regulate HSV-1 gene expression through its receptor via histone modification in cultured neuronal cells.

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