Epstein-Barr virus-derived plasmids replicate only once per cell cycle and are not amplified after entry into cells

Yates, John L.; Guan, Nin

doi:10.1128/jvi.65.1.483-488.1991

Cited by 272 publications

(95 citation statements)

References 29 publications

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“…Our results show that Eland E2-dependent stable replication of the BPV-1 origin is consistent with a random mode of replication, and consequently that once-per-cell cycle replication is not a prerequisite for stable replication. These data indicate that BPV-1 plasmids utilize a completely different set of control mechanisms compared with EBV, which replicates strictly once-per-cell cycle (Yates and Guan, 1991). In contrast to EBV, BPV-1 origin plasmids behave more like bacterial plasmids and are uncoupled from the strict control of initiation of host DNA synthesis.…”

Section: Mode Of Replicationmentioning

confidence: 90%

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Cis and trans requirements for stable episomal maintenance of the BPV-1 replicator.

et al. 1996

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Papillomavirus genomes are maintained as multicopy nuclear plasmids in transformed cells. To address the mechanisms by which the viral DNA is stably propagated in the transformed cells, we have constructed a cell line CH04.15 expressing constitutively the viral proteins E1 and E2, that are required for initiation of viral DNA replication. We show that these viral proteins are necessary and sufficient for stable extrachromosomal replication. Using the cell line CH04.15, we have shown that the bovine papillomavirus‐1 (BPV‐1) minimal origin of replication (MO) is absolutely necessary, but is not sufficient for stable extrachromosomal replication of viral plasmids. By deletion and insertion analysis, we identified an additional element (minichromosome maintenance element, MME) in the upstream regulatory region of BPV‐1 which assures stable replication of the MO‐containing plasmids. This element is composed of multiple binding sites for the transcription activator E2. MME appears to function in the absence of replication but requires E1 and E2 proteins for activity. In contrast to, for example, Epstein‐Barr virus oriP, stably maintained BPV‐1 plasmids are not subject to once‐per‐cell cycle replication as determined by density labelling experiments. These results indicate that papillomavirus episomal replicators replicate independently of the chromosomal DNA of their hosts.

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Section: Mode Of Replicationmentioning

confidence: 90%

“…BrdU labelling and analysis of the replication mode Cells were labelled with 35 .tg/ml BrdU in MEM medium, containing 2'-deoxycytidine (20 ,ug/ml) using procedures described earlier (Yates and Guan, 1991). Episomal and chromosomal DNA was extracted at the times indicated in the Results section.…”

Section: Copy Number Measurementmentioning

confidence: 99%

Cis and trans requirements for stable episomal maintenance of the BPV-1 replicator.

et al. 1996

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“…18,19 This is particularly germane to episomal Tax and similar to episomal sequences of other viruses-for example, those of latent Epstein-Barr virus. 20 Even if Tax is integrated into the genome of the carrier cell, the integration site is known to vary. 21 Of even greater interest are a large number of studies showing that Tax can activate many cellular genes by a process called transactivation.…”

Section: The Human T Cell Lymphotropic Virus Type Imentioning

confidence: 99%

The Role of Human T Cell Lymphotropic Virus Type I Tax in the Development of Cutaneous T Cell Lymphoma

Zucker‐Franklin

2001

Annals of the New York Academy of Sciences

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Although it has been well established that the human T cell lymphotropic virus type I (HTLV‐I) causes adult T cell leukemia/lymphoma (ATLL) in regions of the world where this virus is endemic, its role in the pathogenesis of cutaneous T cell lymphoma (CTCL) in the Western world has been less well established. Most patients with CTCL are negative for antibodies to the structural proteins of HTLV‐I, and thus a causative role for this virus is usually dismissed. However, the Tax sequence of HTLV‐I has been found in the peripheral blood mononuclear cells of practically all patients with CTCL. Such patients express Tax mRNA and have antibodies to p40Tax, the protein encoded by this sequence. Sequence analysis of a 159‐bp region of Tax extracted from CTCL cells proved to be homologous with the same region prepared from a cell line infected with prototypic HTLV‐I. By in situ PCR, Tax has been demonstrated in the lymphocytes infiltrating the skin as well as in the keratinocytes of such patients. Apart from the pathophysiologic and clinical interest of these studies, these observations may have therapeutic implications. In vitro, the proliferation of HTLV‐I‐transformed cells can be inhibited by antisense to HTLV‐I Tax. Since Tax has not been identified in the normal human genome, antisense to Tax deserves serious consideration as a treatment modality for patients whose cells have been demonstrated to harbor Tax.

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“…EBV replication is under the control of some host and viral factors that are not fully understood. EBNA1 plays a key role in the replication and mitotic segregation of EBV DNA episomes to daughter cells (Yates and Guan, 1991;Frappier, 2012b). EBNA1-mediated S-phase episome replication depends on binding of EBNA1 to the EBV origin of genome replication (oriP) (Reisman et al, 1985).…”

Section: Introductionmentioning

confidence: 99%

Epstein-Barr Virus Nuclear Antigen 1 Recruits Cyclophilin A to Facilitate the Replication of Viral DNA Genome

Xin

Liu

et al. 2019

Front. Microbiol.

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Epstein-Barr virus (EBV) nuclear antigen 1 (EBNA1)-mediated DNA episomal genome replication and persistence are essential for the viral pathogenesis. Cyclophilin A (CYPA) is upregulated in EBV-associated nasopharyngeal carcinoma (NPC) with unknown roles. In the present approach, cytosolic CYPA was found to be bound with EBNA1 into the nucleus. The amino acid 376-459 of the EBNA1 domain was important for the binding. CYPA depletion attenuated and ectopic CYPA expression improved EBNA1 expression in EBV-positive cells. The loss of viral copy number was also accelerated by CYPA consumption in daughter cells during culture passages. Mechanistically, CYPA mediated the connection of EBNA1 with oriP (origin of EBV DNA replication) and subsequent oriP transcription, which is a key step for the initiation of EBV genome replication. Moreover, CYPA overexpression markedly antagonized the connection of EBNA1 to Ubiquitinspecific protease 7 (USP7), which is a strong host barrier with a role of inhibiting EBV genome replication. The PPIase activity of CYPA was required for the promotion of oriP transcription and antagonism with USP7. The results revealed a strategy that EBV recruited a host factor to counteract the host defense, thus facilitating its own latent genome replication. This study provides a new insight into EBV pathogenesis and potential virus-targeted therapeutics in EBV-associated NPC, in which CYPA is upregulated at all stages.

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Epstein-Barr virus-derived plasmids replicate only once per cell cycle and are not amplified after entry into cells

Cited by 272 publications

References 29 publications

Cis and trans requirements for stable episomal maintenance of the BPV-1 replicator.

Cis and trans requirements for stable episomal maintenance of the BPV-1 replicator.

The Role of Human T Cell Lymphotropic Virus Type I Tax in the Development of Cutaneous T Cell Lymphoma

Epstein-Barr Virus Nuclear Antigen 1 Recruits Cyclophilin A to Facilitate the Replication of Viral DNA Genome

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