Identification of a Second ATF/CREB-like Element in the Herpes Simplex Virus Type 1 (HSV-1) Latency-Associated Transcript (LAT) Promoter

Kenny, Joseph J.; Krebs, Fred C.; Hartle, Heather T.; Gartner, Amy E.; Chatton, Bruno; Leiden, Jeffrey M.; Hoeffler, James P.; Weber, Peter; Wigdahl, Brian

doi:10.1006/viro.1994.1180

Cited by 43 publications

(38 citation statements)

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“…Nevertheless, many aspects of HSV-1 transcriptional regulation during lytic infection have been shown to be highly similar to that of and to require factors from the mammalian host. For example, HSV-1 genes utilize many host transcriptional activators, such as Oct1, Sp1, and CREB (15,16,25,41), and these activators interact with chromatin-modulating enzymes (1,5). Taken together, these data led us to reexamine the nucleosomal state of lytically infecting HSV-1 DNA in human neuroblastoma (Sy5y) cells.…”

Section: Discussionmentioning

confidence: 99%

During Lytic Infection Herpes Simplex Virus Type 1 Is Associated with Histones Bearing Modifications That Correlate with Active Transcription

Kent

Zeng

Atanasiu

et al. 2004

J Virol

151

182

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Herpes simplex virus type 1 (HSV-1) is a large (150-kb) double-stranded DNA virus that forms latent infections in neuronal cells of the human peripheral nervous system. Previous work determined that the HSV-1 genome is found in an ordered nucleosomal structure during latent infection. However, during lytic infection, it was unclear whether viral DNA was in a chromatin state. We examined HSV-1 during lytic infection using micrococcal nuclease digestion and chromatin immunoprecipitation. The HSV-1 genome is at least partially nucleosomal, although apparently not in a regular repeating structure. Analysis of histones associated with HSV-1, within both the promoter and the transcribed regions, revealed covalent amino tail modifications similar to those associated with active host mammalian genes. Certain of the modifications were detected in the temporal order expected of the immediate-early, early, and late gene classes. These data suggest that productive infection may be accompanied by acquisition of a permissive chromatin state.

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Section: Discussionmentioning

confidence: 99%

During Lytic Infection Herpes Simplex Virus Type 1 Is Associated with Histones Bearing Modifications That Correlate with Active Transcription

Kent

Zeng

Atanasiu

et al. 2004

J Virol

151

182

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“…Many of these transcription factors are present in nonneural cells and thus have the potential to activate expression in transiently transfected cells. For example, the two cyclic AMP (cAMP)-responsive element (CRE)-binding sites in the LAT promoter are functional because cAMP activates the promoter (122,141). The CRE motif that is proximal to the TATA box is important for expression in neurons, and its presence has a positive effect on reactivation from latency (15,141,207).…”

Section: The Promoter That Regulates Lat Expression Is a Neuronspecifmentioning

confidence: 99%

Herpes Simplex Virus Type 1 and Bovine Herpesvirus 1 Latency

2003

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Primary infection by herpes simplex virus type 1 (HSV-1) can cause clinical symptoms in the peripheral and central nervous system, upper respiratory tract, and gastrointestinal tract. Recurrent ocular shedding leads to corneal scarring that can progress to vision loss. Consequently, HSV-1 is the leading cause of corneal blindness due to an infectious agent. Bovine herpesvirus 1 (BHV-1) has similar biological properties to HSV-1 and is a significant health concern to the cattle industry. Latency of BHV-1 and HSV-1 is established in sensory neurons of trigeminal ganglia, but latency can be interrupted periodically, leading to reactivation from latency and spread of infectious virus. The ability of HSV-1 and BHV-1 to reactivate from latency leads to virus transmission and can lead to recurrent disease in individuals latently infected with HSV-1. During latency, the only abundant HSV-1 RNA expressed is the latency-associated transcript (LAT). In latently infected cattle, the latency-related (LR) RNA is the only abundant transcript that is expressed. LAT and LR RNA are antisense to ICP0 or bICP0, viral genes that are crucial for productive infection, suggesting that LAT and LR RNA interfere with productive infection by inhibiting ICP0 or bICP0 expression. Numerous studies have concluded that LAT expression is important for the latency-reactivation cycle in animal models. The LR gene has recently been demonstrated to be required for the latency-reactivation cycle in cattle. Several recent studies have demonstrated that LAT and the LR gene inhibit apoptosis (programmed cell death) in trigeminal ganglia of infected animals and transiently transfected cells. The antiapoptotic properties of LAT map to the same sequences that are necessary for promoting reactivation from latency. This review summarizes our current knowledge of factors regulating the latency-reactivation cycle of HSV-1 and BHV-1

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“…The HSV-1 LAT promoter also contains two putative CREs, CRE1 (26) and CRE2 (20). A mutation in CRE1 in the context of the viral genome reduces reactivation of virus by epinephrine iontophoresis (4), and in a rat pheochromocytoma cell line it confers cyclic AMP responsiveness to the LAT promoter (26).…”

Section: Luman Protects Cells From a Productive Infection By Hsv-1mentioning

confidence: 99%

Potential Role for Luman, the Cellular Homologue of Herpes Simplex Virus VP16 (α Gene trans -Inducing Factor), in Herpesvirus Latency

Misra

2000

J Virol

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The cascade of herpes simplex virus (HSV) gene expression that results in viral replication begins with the activation of viral immediate-early (IE) genes by the virion-associated protein VP16. VP16 on its own is inefficient at associating with complexes formed on IE gene promoters and depends upon the cellular factor HCF for its activity. In this respect VP16 mimics the host basic leucine zipper (bZIP) protein Luman, which also requires HCF for activating transcription. Our objective is to explore interactions between Luman and HCF and to determine if they play a role in the biology of herpesviruses. In this report we show that in cultured cells ectopically expressed Luman was retained in the cytoplasm, where it colocalized with Calnexin, a protein normally associated with the endoplasmic reticulum (ER). Retention of Luman in the ER depends on a hydrophobic segment of the protein that probably serves as a transmembrane domain. Deletion of this domain changed the intracellular location of Luman so that most of the mutant protein was in the nucleus of cells. While HCF was present in the nucleus of most cells, in cells expressing Luman it was retained in the cytoplasm where the two proteins colocalized. This cytoplasmic association of Luman and HCF could also be demonstrated in neurons in trigeminal ganglia removed from cattle soon after death. Cells in tissue culture that expressed Luman, but not a mutant form of the protein that fails to bind HCF, were resistant to a productive infection with HSV type 1 (HSV-1). We hypothesize that similar Luman-HCF interactions in sensory neurons in trigeminal ganglia result in the suppression of viral replication and the establishment of latency. Interestingly, Luman could activate the promoters of IE110 and LAT, two genes that are critical for reactivation of HSV-1 from latency. This suggests a role for Luman in the reactivation process as well.Infection for the first time with an alphaherpesvirus leads to active replication of the virus in epithelial cells at the portal of entry. The virus spreads to adjoining cells but also enters the termini of sensory nerves, innervating the site of replication. It is then transported along axons to neuronal cell bodies in sensory ganglia, where it establishes a latent infection. The virus is relatively quiescent during the latent state but is reactivated periodically to replicate and move back down the axons to reinfect epithelial surfaces (reviewed in reference 42).Herpes simplex virus type 1 (HSV-1) and Bovine herpesvirus type 1 (BHV-1) are alphaherpesviruses that usually cause primary infections in epithelia of the oropharynx and face. The main sites of latency for these viruses are neurons in the trigeminal ganglia (recently reviewed by Jones [18]). During latent infections by HSV-1 and BHV-1, transcripts arising from only a small portion of the viral genomes (LAT or LRG, respectively) can be detected in neurons. The exact role of these transcripts in the establishment of the latent infection and in reactivation from it is unclear. H...

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Identification of a Second ATF/CREB-like Element in the Herpes Simplex Virus Type 1 (HSV-1) Latency-Associated Transcript (LAT) Promoter

Cited by 43 publications

References 0 publications

During Lytic Infection Herpes Simplex Virus Type 1 Is Associated with Histones Bearing Modifications That Correlate with Active Transcription

During Lytic Infection Herpes Simplex Virus Type 1 Is Associated with Histones Bearing Modifications That Correlate with Active Transcription

Herpes Simplex Virus Type 1 and Bovine Herpesvirus 1 Latency

Potential Role for Luman, the Cellular Homologue of Herpes Simplex Virus VP16 (α Gene trans -Inducing Factor), in Herpesvirus Latency

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