Epstein-Barr Virus Lytic Cycle Reactivation

McKenzie, Jessica; El-Guindy, Ayman

doi:10.1007/978-3-319-22834-1_8

Cited by 80 publications

(100 citation statements)

References 202 publications

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“…EBV early genes are synergistically induced by ZTA and RTA and encode the viral polymerase and replication machinery. Late viral genes encode structural proteins that encapsidate and mediate release of infectious virions (McKenzie and El-Guindy, 2015). …”

Section: Introductionmentioning

confidence: 99%

A Temporal Proteomic Map of Epstein-Barr Virus Lytic Replication in B Cells

et al. 2017

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SummaryEpstein-Barr virus (EBV) replication contributes to multiple human diseases, including infectious mononucleosis, nasopharyngeal carcinoma, B cell lymphomas, and oral hairy leukoplakia. We performed systematic quantitative analyses of temporal changes in host and EBV proteins during lytic replication to gain insights into virus-host interactions, using conditional Burkitt lymphoma models of type I and II EBV infection. We quantified profiles of >8,000 cellular and 69 EBV proteins, including >500 plasma membrane proteins, providing temporal views of the lytic B cell proteome and EBV virome. Our approach revealed EBV-induced remodeling of cell cycle, innate and adaptive immune pathways, including upregulation of the complement cascade and proteasomal degradation of the B cell receptor complex, conserved between EBV types I and II. Cross-comparison with proteomic analyses of human cytomegalovirus infection and of a Kaposi-sarcoma-associated herpesvirus immunoevasin identified host factors targeted by multiple herpesviruses. Our results provide an important resource for studies of EBV replication.

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Section: Introductionmentioning

confidence: 99%

A Temporal Proteomic Map of Epstein-Barr Virus Lytic Replication in B Cells

et al. 2017

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“…The molecular mechanisms driving the process of reactivation are understood primarily in the context of transcriptional regulation of the BZLF1 promoter (Zp). Numerous factors that bind to Zp have been identified as either positive or negative regulators of BZLF1 transcription, as well as a few cellular factors that contribute to lytic reactivation (McKenzie and El-Guindy, 2015). Understanding the molecular mechanisms dictating the latent to lytic switch may offer therapeutic insight for oncolytic therapy in latency-associated tumors.…”

Section: Introductionmentioning

confidence: 99%

PARP1 restricts Epstein Barr Virus lytic reactivation by binding the BZLF1 promoter

et al. 2017

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The Epstein Barr virus (EBV) genome persists in infected host cells as a chromatinized episome and is subject to chromatin-mediated regulation. Binding of the host insulator protein CTCF to the EBV genome has an established role in maintaining viral latency type, and in other herpesviruses, loss of CTCF binding at specific regions correlates with viral reactivation. Here, we demonstrate that binding of PARP1, an important cofactor of CTCF, at the BZLF1 lytic switch promoter restricts EBV reactivation. Knockdown of PARP1 in the Akata-EBV cell line significantly increases viral copy number and lytic protein expression. Interestingly, CTCF knockdown has no effect on viral reactivation, and CTCF binding across the EBV genome is largely unchanged following reactivation. Moreover, EBV reactivation attenuates PARP activity, and Zta expression alone is sufficient to decrease PARP activity. Here we demonstrate a restrictive function of PARP1 in EBV lytic reactivation.

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“…274,275 In cells supporting Epstein-Barr virus lytic replication, more than 100 viral gene products are expressed, which in turn choreograph extensive cellular events to impact cell growth and proliferation. 276…”

Section: Latency Of Epstein-barr Virus Converts To a Lytic Cycle By Amentioning

confidence: 99%

Herpesvirus‐bacteria synergistic interaction in periodontitis

Chen

Feng

Slots

2019

Periodontology 2000

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The etiopathogenesis of severe periodontitis includes herpesvirus‐bacteria coinfection. This article evaluates the pathogenicity of herpesviruses (cytomegalovirus and Epstein‐Barr virus) and periodontopathic bacteria (Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis) and coinfection of these infectious agents in the initiation and progression of periodontitis. Cytomegalovirus and A. actinomycetemcomitans/P. gingivalis exercise synergistic pathogenicity in the development of localized (“aggressive”) juvenile periodontitis. Cytomegalovirus and Epstein‐Barr virus are associated with P. gingivalis in adult types of periodontitis. Periodontal herpesviruses that enter the general circulation may also contribute to disease development in various organ systems. A 2‐way interaction is likely to occur between periodontal herpesviruses and periodontopathic bacteria, with herpesviruses promoting bacterial upgrowth, and bacterial factors reactivating latent herpesviruses. Bacterial‐induced gingivitis may facilitate herpesvirus colonization of the periodontium, and herpesvirus infections may impede the antibacterial host defense and alter periodontal cells to predispose for bacterial adherence and invasion. Herpesvirus‐bacteria synergistic interactions, are likely to comprise an important pathogenic determinant of aggressive periodontitis. However, mechanistic investigations into the molecular and cellular interaction between periodontal herpesviruses and bacteria are still scarce. Herpesvirus‐bacteria coinfection studies may yield significant new discoveries of pathogenic determinants, and drug and vaccine targets to minimize or prevent periodontitis and periodontitis‐related systemic diseases.

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Epstein-Barr Virus Lytic Cycle Reactivation

Cited by 80 publications

References 202 publications

A Temporal Proteomic Map of Epstein-Barr Virus Lytic Replication in B Cells

A Temporal Proteomic Map of Epstein-Barr Virus Lytic Replication in B Cells

PARP1 restricts Epstein Barr Virus lytic reactivation by binding the BZLF1 promoter

Herpesvirus‐bacteria synergistic interaction in periodontitis

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