Analysis of the transcriptional promoter which regulates the latency-related transcript of bovine herpesvirus 1

Jones, Clinton; Delhon, G.; Bratanich, Ana; Kutish, G. F.; Rock, Daniel L.

doi:10.1128/jvi.64.3.1164-1170.1990

Cited by 46 publications

(39 citation statements)

References 18 publications

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“…This is consistent with a previous study that concluded that the number of LRT-positive trigeminal ganglionic neurons decreased when latently infected rabbits were injected with DEX (23). DEX also represses the LRT promoter activity in transiently transfected bovine cells (14). Thus, repression of LRT by DEX in tonsils and TG correlates with reactivation.…”

Section: Discussionsupporting

confidence: 92%

Persistence and Reactivation of Bovine Herpesvirus 1 in the Tonsils of Latently Infected Calves

Winkler¹,

Doster²,

Jones³

2000

J. Virol.

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Bovine herpesvirus 1 (BHV-1), like other members of the Alphaherpesvirinae subfamily, establishes latent infection in sensory neurons. Reactivation from latency can occur after natural or corticosteroid-induced stress culminating in recurrent disease and/or virus transmission to uninfected animals. Our previous results concluded that CD4 ؉ T cells in the tonsil and other adjacent lymph nodes are infected and undergo apoptosis during acute infection (M. T. Winkler, A. Doster, and C. Jones, J. Virol. 73:8657-8668, 1999). To test whether BHV-1 persisted in lymphoreticular tissue, we analyzed tonsils of latently infected calves for the presence of viral DNA and gene expression. BHV-1 DNA was consistently detected in the tonsils of latently infected calves. Detection of the latency-related transcript (LRT) in tonsils of latently infected calves required nested reverse transcription-PCR (RT-PCR) suggesting that only a few cells contained viral DNA or that LRT is not an abundant transcript. bICP0 (immediate-early and early transcripts), ribonucleotide reductase (early transcript), and glycoprotein C (late transcript) were not detected by RT-PCR in latently infected calves. When reactivation was initiated by dexamethasone, bICP0 and ribonucleotide reductase transcripts were detected.Following dexamethasone treatment, viral nucleic acid was detected simultaneously in trigeminal ganglionic neurons and lymphoid follicles of tonsil. LRT was detected at 6 and 24 h after dexamethasone treatment but not at 48 h. Dexamethasone-induced reactivation led to apoptosis that was localized to tonsillar lymphoid follicles. Taken together, these findings suggest that the tonsil is a site for persistence or latency from which virus can be reactivated by dexamethasone. We further hypothesize that the shedding of virus from the tonsil during reactivation plays a role in virus transmission.

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Section: Discussionsupporting

confidence: 92%

Persistence and Reactivation of Bovine Herpesvirus 1 in the Tonsils of Latently Infected Calves

Winkler¹,

Doster²,

Jones³

2000

J. Virol.

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“…One small region of the genome is transcriptionally active in latently infected neurons, and this region is designated the latency-related gene (LRG). The results of previous studies revealed that expression of the LRG is controlled by a 980-nucleotide (980-nt) fragment (3,4,16). During a productive infection in bovine cells, the transcriptional start site for LR RNA is downstream of two TATA elements (3).…”

mentioning

confidence: 99%

“…Although the LR promoter has been analyzed in considerable detail (3,4,16), it is not known whether a protein is synthesized from the LRG. The aim of this work was to determine if the LRG can encode a protein.…”

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confidence: 99%

Identification of gene products encoded by the latency-related gene of bovine herpesvirus 1

Hossain

Schang

Jones

1995

J Virol

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Bovine herpesvirus 1 (BHV-1) establishes a latent infection in sensory ganglionic neurons of infected animals. Expression of latency-related (LR) gene products is controlled by a 980-bp fragment (LR promoter).DNA sequence analysis revealed that two major open reading frames (ORFs) are in the LR gene. Antibodies directed against both ORFs were generated in rabbits by using synthetic peptides. Antibody P2, which is directed to sequences near the amino terminus of ORF 2, recognized a 41-kDa protein in lytically infected cells, suggesting that ORF 2 encodes a protein. When the LR gene was inserted into a mammalian expression vector and subsequently transfected into COS-7 cells, a 41-kDa protein was detected by use of silver-stained sodium dodecyl sulfate-polyacrylamide gels and by the P2 antibody. In contrast, this protein was not detected in mock-transfected cells. Deletion of DNA sequences containing ORF 2 blocked synthesis of the 41-kDa protein in COS-7 cells. Reverse transcriptase-mediated PCRs indicated that splicing occurs near the C terminus of ORF 2. Further studies indicated that LR RNA was alternatively spliced in latently infected cattle and that a fraction of LR RNA was poly(A) ؉ . Taken together, these studies suggested that a spliced LR transcript has the potential to encode a 41-kDa protein.

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“…A DMSO or glycerol shock was not used because this treatment alters TPA response as well as pristane response in chloramphenicol acetyltransferase (CAT) assays [21]. Forty hours after transfection, the cells were washed three times with phosphate-buffered saline (PBS), and a cell lysate was prepared by three freeze-thaw cycles in 0.25 M Tris, pH 7.8, as described previously [32,33]. CAT enzymatic activity was measured in a reaction containing 0.2 pCi of ['4C]chloramphenicol (45 mCi/mmol); 100 mM Tris-HCI, pH 7.8; and 0.5 mM acetyl-CoA.…”

Section: Measurement Of Chloramphenicol Acetyltransferase Activity Inmentioning

confidence: 99%

Analysis of transcriptional activation of a cyclic AMP response element by 2,6,10,14‐tetramethylpentadecane (pristane) in JB6 mouse epidermal cells

Bańbura

Ackland-Berglund

Lee

et al. 1994

Molecular Carcinogenesis

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Pristane is a naturally occurring isoprenoid that is believed to be derived from the phytyl moiety of chlorophyll. Thus, it is not surprising that pristane is present in many common fruits and vegetables. Furthermore, pristane can be detected in the tissues of fish and mammals. In animal models using rodents, pristane can function as a potent tumor promoter. At the molecular level, pristane can induce changes in the plasma membrane, alter the conformation of chromatin, and selectively activate gene expression. Addition of pristane to a mouse epidermal cell line (JB6 P+) allows these cells to grow in an anchorage-independent manner. In contrast, JB6 P-cells are not transformed by pristane. Our study was undertaken to correlate transformation of P+ cells with changes induced by pristane. Transcriptional activation of a cyclic AMP response element (CRE) was induced by pristane in P+ and P-cells. Point mutations in the CRE abolished activation by pristane, thus indicating that an intact CRE was necessary for pristane activation. In P+ cells, pristane repressed phosphodiesterase activity. However, protein kinase A was activated by pristane in P+ and P-cells. Taken together, these results indicated pristane induced novel changes in P+ cells that in turn may facilitate neoplastic transformation.

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Analysis of the transcriptional promoter which regulates the latency-related transcript of bovine herpesvirus 1

Cited by 46 publications

References 18 publications

Persistence and Reactivation of Bovine Herpesvirus 1 in the Tonsils of Latently Infected Calves

Persistence and Reactivation of Bovine Herpesvirus 1 in the Tonsils of Latently Infected Calves

Identification of gene products encoded by the latency-related gene of bovine herpesvirus 1

Analysis of transcriptional activation of a cyclic AMP response element by 2,6,10,14‐tetramethylpentadecane (pristane) in JB6 mouse epidermal cells

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