Requirement of a 12-Base-Pair TATT-Containing Sequence and Viral Lytic DNA Replication in Activation of the Kaposi's Sarcoma-Associated Herpesvirus K8.1 Late Promoter

Tang, Shuang; Yamanegi, Koji; Zheng, Zhi-Ming

doi:10.1128/jvi.78.5.2609-2614.2004

Cited by 47 publications

(54 citation statements)

References 32 publications

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“…The PAA sensitivity of ORF19 mRNA accumulation in latently infected cells is indicative of a true late gene. Studies of other examples have identified a TA-rich element that is important for promoter activity (5,43,51,56,68). Examination of the ORF19hp sequence identified an 8 of 12 bp match (Fig.…”

Section: Resultsmentioning

confidence: 99%

Wide-Scale Use of Notch Signaling Factor CSL/RBP-Jκ in RTA-Mediated Activation of Kaposi's Sarcoma-Associated Herpesvirus Lytic Genes

Persson

Wilson

2010

J Virol

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Section: Resultsmentioning

confidence: 99%

Wide-Scale Use of Notch Signaling Factor CSL/RBP-Jκ in RTA-Mediated Activation of Kaposi's Sarcoma-Associated Herpesvirus Lytic Genes

Persson

Wilson

2010

J Virol

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“…To establish an analogous system for KSHV, we cloned the KSHV K8.1 late gene promoter or, as controls, the K14 and ORF57 early gene promoters upstream of a firefly luciferase reporter gene (5). Cotransfection of the six KSHV vTFs with the luciferase reporter plasmid led to specific activation of the late K8.1 promoter, whereas the six vTFs had no effect on the KSHV K14 or ORF57 early promoter (Fig.…”

Section: R328amentioning

confidence: 99%

“…n betaherpesviruses and gammaherpesviruses, mapped promoters driving late gene transcription are strikingly minimal and their activation is dependent on a set of conserved viral transcription regulatory proteins (1)(2)(3)(4)(5)(6)(7)(8). Studies of the gammaherpesviruses murine gammaherpesvirus 68 (MHV68), Epstein-Barr virus (EBV), and Kaposi's sarcoma-associated herpesvirus (KSHV), as well as the betaherpesvirus human cytomegalovirus (HCMV), identified six viral transactivation factors (vTFs), open reading frame 18 (ORF18), ORF24, ORF30, ORF31, ORF34, and ORF66 (gammaherpesvirus nomenclature) necessary for late gene expression (1-4, 6, 7, 9, 10).…”

mentioning

confidence: 99%

Interaction between ORF24 and ORF34 in the Kaposi's Sarcoma-Associated Herpesvirus Late Gene Transcription Factor Complex Is Essential for Viral Late Gene Expression

Davis

Hesser

Park

et al. 2016

J Virol

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Transcription of herpesviral late genes is stimulated after the onset of viral DNA replication but otherwise restricted. Late gene expression in gammaherpesviruses requires the coordination of six early viral proteins, termed viral transactivation factors (vTFs). Here, we mapped the organization of this protein complex for Kaposi's sarcoma-associated herpesvirus. Disruption of this complex via point mutation of the interaction interface between the open reading frame 24 (ORF24) and ORF34 vTFs ablated both late gene expression and viral replication.

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“…The luciferase reporters were cotransfected with pRL-Ts, a Renilla luciferase reporter (36). The dual-luciferase assay was performed with a dual-luciferase assay kit (Promega) as described previously (36). The firefly luciferase activity was normalized to the Renilla luciferase activity.…”

Section: Methodsmentioning

confidence: 99%

“…Plasmids and RNA oligonucleotides were transfected into 293 cells using Lipofectamine 2000 (Life Technologies) according to the manufacturer's instructions. The luciferase reporters were cotransfected with pRL-Ts, a Renilla luciferase reporter (36). The dual-luciferase assay was performed with a dual-luciferase assay kit (Promega) as described previously (36).…”

Section: Methodsmentioning

confidence: 99%

Characterization of Herpes Simplex Virus 2 Primary MicroRNA Transcript Regulation

Tang

Bosch–Marcé

Patel

et al. 2015

J Virol

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In order to understand factors that may influence latency-associated transcription and latency-associated transcript (LAT) phenotypes, we studied the expression of the herpes simplex virus 2 (HSV-2) LAT-associated microRNAs (miRNAs). We mapped the transcription initiation sites of all three primary miRNA transcripts and identified the ICP4-binding sequences at the transcription initiation sites of both HSV-2 LAT (pri-miRNA for miR-I and miR-II, which target ICP34.5, and miR-III, which targets ICP0) and L/ST (a pri-miRNA for miR-I and miR-II) but not at that of the primary miR-H6 (for which the target is unknown). We confirmed activity of the putative HSV-2 L/ST promoter and found that ICP4 trans-activates the L/ST promoter when the ICP4-binding site at its transcription initiation site is mutated, suggesting that ICP4 may play a dual role in regulating transcription of L/ST and, consequently, of miR-I and miR-II. LAT exon 1 (containing LAT enhancer sequences), together with the LAT promoter region, comprises a bidirectional promoter required for the expression of both LAT-encoded miRNAs and miR-H6 in latently infected mouse ganglia. The ability of ICP4 to suppress ICP34.5-targeting miRNAs and to activate lytic viral genes suggests that ICP4 could play a key role in the switch between latency and reactivation. IMPORTANCEThe HSV-2 LAT and viral miRNAs expressed in the LAT region are the most abundant viral transcripts during HSV latency. The balance between the expression of LAT and LAT-associated miRNAs and the expression of lytic viral transcripts from the opposite strand appears to influence whether individual HSV-infected neurons will be latently or productively infected. The outcome of neuronal infection may thus depend on regulation of gene expression of the corresponding primary miRNAs. In the present study, we characterize promoter sequences responsible for miRNA expression, including identification of the primary miRNA 5= ends and evaluation of ICP4 response. These findings provide further insight into the virus' strategy to tightly control expression of lytic cycle genes (especially the neurovirulence factor, ICP34.5) and suggest a mechanism (via ICP4) for the transition from latency to reactivated productive infection. Herpes simplex virus 1 (HSV-1) and HSV-2 are closely related herpesviruses. HSV-1 typically infects the facial region and establishes a lifelong latent infection in sensory neurons of the trigeminal ganglia (TG), while HSV-2 typically infects the genital region and establishes a lifelong latent infection in sensory neurons of the sacral dorsal root ganglia. Periodically, either virus may reactivate to cause symptomatic or asymptomatic recurrences in the area served by these sensory neurons.Both HSV-2 and HSV-1 acutely and latently express miRNAs, which are proposed to play an important role in regulating whether an infection will be productive or latent. These miRNAs, which are conserved more in location than in sequence (1, 2, 9, 10), reduce expression of viral genes transcribed ...

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Requirement of a 12-Base-Pair TATT-Containing Sequence and Viral Lytic DNA Replication in Activation of the Kaposi's Sarcoma-Associated Herpesvirus K8.1 Late Promoter

Cited by 47 publications

References 32 publications

Wide-Scale Use of Notch Signaling Factor CSL/RBP-Jκ in RTA-Mediated Activation of Kaposi's Sarcoma-Associated Herpesvirus Lytic Genes

Wide-Scale Use of Notch Signaling Factor CSL/RBP-Jκ in RTA-Mediated Activation of Kaposi's Sarcoma-Associated Herpesvirus Lytic Genes

Interaction between ORF24 and ORF34 in the Kaposi's Sarcoma-Associated Herpesvirus Late Gene Transcription Factor Complex Is Essential for Viral Late Gene Expression

Characterization of Herpes Simplex Virus 2 Primary MicroRNA Transcript Regulation

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