scholarly journals A cancer-associated Epstein-Barr virus BZLF1 promoter variant enhances lytic infection

2018 ◽  
Vol 14 (7) ◽  
pp. e1007179 ◽  
Author(s):  
Jillian A. Bristol ◽  
Reza Djavadian ◽  
Emily R. Albright ◽  
Carrie B. Coleman ◽  
Makoto Ohashi ◽  
...  
Keyword(s):  
Epstein Barr Virus ◽  
Lytic Infection ◽  
Barr Virus ◽  
Epstein Barr ◽  
Bzlf1 Promoter

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

Virology ◽  
2017 ◽  
Vol 507 ◽  
pp. 220-230 ◽  
Author(s):  
Lena N. Lupey-Green ◽  
Stephanie A. Moquin ◽  
Kayla A. Martin ◽  
Shane M. McDevitt ◽  
Michael Hulse ◽  
...  
Keyword(s):  
Epstein Barr Virus ◽  
Barr Virus ◽  
Lytic Reactivation ◽  
Epstein Barr ◽  
Bzlf1 Promoter

scholarly journals Characterization of Proteins Binding to the ZII Element in the Epstein–Barr Virus BZLF1 Promoter: Transactivation by ATF1

Virology ◽  
1997 ◽  
Vol 227 (2) ◽  
pp. 323-330 ◽  
Author(s):  
Yi-Chun James Wang ◽  
Jung-Ming Huang ◽  
Eduardo A. Montalvo
Keyword(s):  
Epstein Barr Virus ◽  
Barr Virus ◽  
Epstein Barr ◽  
Bzlf1 Promoter

scholarly journals Direct evidence of abortive lytic infection-mediated establishment of Epstein-Barr virus latency during B-cell infection

2020 ◽  
Author(s):  
Tomoki Inagaki ◽  
Yoshitaka Sato ◽  
Jumpei Ito ◽  
Mitsuaki Takaki ◽  
Yusuke Okuno ◽  
...  
Keyword(s):  
Viral Infection ◽  
Epstein Barr Virus ◽  
Lytic Infection ◽  
Lytic Gene ◽  
Barr Virus ◽  
Ebv Infection ◽  
Infected Cells ◽  
Epstein Barr ◽  
Viral Responses ◽  
Latent Phase

AbstractViral infection induces dynamic changes in transcriptional profiles. Virus-induced and anti-viral responses are intertwined during the infection. Epstein-Barr virus (EBV) is a human gammaherpesvirus that provides a model of herpesvirus latency. To measure the transcriptome changes during the establishment of EBV latency, EBV-negative Akata cells were infected with EBV-EGFP and observed by transcriptome sequencing (RNA-seq) at 0, 2, 4, 7, 10, and 14 days after infection. We found transient downregulation of mitotic division-related genes, reflecting reprograming of cell growth by EBV. Moreover, a burst of viral lytic gene expression was detected in the early phase of infection. Experimental and mathematical investigations demonstrated that infectious virions were not produced in the pre-latent phase, suggesting the presence of an abortive lytic infection. Finally, we conducted fate mapping using recombinant EBV, enabling the noninvasive, continuous observation of infected cells during EBV infection. Our tracking analysis provided direct evidence that the abortive lytic infection in the pre-latent phase converges to latent infection during EBV infection of B-cells, shedding light on novel roles of viral lytic gene(s) in establishing latency.Author summaryViral infection is a complex process that activates both virus-triggered and host anti-viral responses. This process has classically been studied by snapshot analysis such as microarray and RNA-seq at discrete time points as population averages. Snapshot data lead to invaluable findings in host-pathogen interactions. However, these “snapshot” omics, even from a single cell, lack temporal resolution. Because the behavior of infected cells is highly dynamic and heterogenous, continuous analysis is required for deciphering the fate of infected cells during viral infection. Here, we exploited fate mapping techniques with recombinant Epstein-Barr virus (EBV) to track the infected cells and recorded a log of lytic gene expression during EBV infection. Our continuous observation of infected cells revealed that EBV established latency in B-cells via an abortive lytic infection in the pre-latent phase.

scholarly journals ZEBRA and a Fos-GCN4 chimeric protein differ in their DNA-binding specificities for sites in the Epstein-Barr virus BZLF1 promoter.

1991 ◽  
Vol 65 (8) ◽  
pp. 4033-4041 ◽  
Author(s):  
N Taylor ◽  
E Flemington ◽  
J L Kolman ◽  
R P Baumann ◽  
S H Speck ◽  
...  
Keyword(s):  
Dna Binding ◽  
Epstein Barr Virus ◽  
Chimeric Protein ◽  
Barr Virus ◽  
Epstein Barr ◽  
Bzlf1 Promoter

Characterizing The CpG Methylation Of Epstein-Barr Virus DNA In The Plasma Of Patients With Hodgkin Lymphoma and HIV-Associated Burkitt Lymphoma

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 4232-4232
Author(s):  
Jennifer A. Kanakry ◽  
Meir Shamay ◽  
Yvette L. Kasamon ◽  
Hailun Li ◽  
Randy D. Gascoyne ◽  
...  
Keyword(s):  
Epstein Barr Virus ◽  
Cpg Methylation ◽  
Lytic Infection ◽  
Viral Dna ◽  
Barr Virus ◽  
Methylation Assay ◽  
Latently Infected ◽  
Ebv Dna ◽  
Epstein Barr ◽  
Immunocompromised Hosts

Abstract Background Epstein-Barr virus (EBV) is harbored as latent virus within the tumor cells of a subset of classical Hodgkin lymphoma (HL) and HIV-associated Burkitt lymphoma (BL). In HL, we and others have previously shown that elevated EBV DNA copies in plasma accurately distinguish EBV(+) tumors from EBV(-) tumors. However, EBV DNA may be present in plasma due to apoptosis of latently infected EBV(+) tumor cells (or latent EBV(+) benign lymphocytes), as a result of replicative lytic infection (particularly in immunocompromised hosts), or both. Thus, detecting elevated EBV DNA copies in plasma by does not always signify the presence of an EBV(+) tumor. However, a distinction is that the EBV DNA derived from latently infected cells is replicated by cellular DNA polymerase and is usually CpG methylated, whereas EBV DNA in lytic infection is replicated by the viral DNA polymerase and is never CpG methylated. Methods To improve upon plasma EBV DNA as a tumor-specific marker in EBV(+) lymphomas, we assessed the CpG methylation of EBV DNA in a subset of plasma specimens from immunocompetent patients with HL (enrolled in the Eastern Cooperative Oncology Group E2496 trial) and a subset from patients with HIV-associated BL (enrolled in the AIDS Malignancy Consortium 048 trial). The EBV tumor status was determined by in situ hybridization (ISH) on tissue for EBV RNAs (EBER). For the CpG methylation assay, methyl binding domain paramagnetic beads were used to first fractionate CpG methylated DNA from CpG unmethylated DNA in plasma. EBV DNA in each fraction were quantified by real time polymerase chain reaction (qPCR) to determine the percentage of methylated EBV DNA. Specimens with > 100 EBV DNA copies/mL plasma were analyzed. Results Among patients with EBER(+) HL and elevated EBV DNA in plasma prior to therapy (n=8), EBV DNA was largely CpG methylated (median 95%, range 54%-99%). By contrast, in the rare cases where patients with EBER(-) HL tumors had high EBV DNA copy number in plasma prior to therapy (4 of 92, 4%), only small percentages of EBV DNA were methylated in 3 patients (5%, 9%, and 12%). In the fourth patient, the plasma EBV DNA was 99% CpG methylated. We suspect that patient 4 had an EBV-associated HL with either a technical failure of EBER-ISH or an instance of a tumor that harbors viral DNA but does not express EBERs. In patients with HIV-associated BL, plasma EBV DNA copies were elevated in 100% of patients with EBER(+) BL (n=4), but also in 4 of 9 (56%) patients with EBER(-) BL. This propensity to detect EBV DNA in the plasma of patients with HIV but without EBV(+) BL likely reflects replicative lytic infection in immunocompromised hosts, making plasma EBV DNA less reliable as a marker of EBV(+) lymphoma in this setting. Thus, we applied the methylation assay to specimens from patients with HIV and BL. Patients with HIV and EBER(+) BL tumors (n=4), EBV DNA was 28%, 46%, 47%, and 60% methylated, whereas a patient with HIV and EBER(-) BL had lower methylation at 8%. To better elucidate the meaning of plasma EBV DNA elevations during lymphoma treatment, we applied the methylation assay to specimens from patients with EBV(+) HL and elevated EBV DNA in plasma at month 6 of therapy (n=4). Dense CpG methylation (96%) of plasma EBV DNA was detected in 1 patient who went on to relapse at Month 15, while the plasma EBV DNA was largely unmethylated in 3 patients who remain in remission each with over 5 years of follow-up. Conclusion In settings where EBV DNA is detected in plasma, the CpG methylation assay helps differentiate patients with EBV(+) HL or BL from those with EBV(-) tumors. In patients with HIV where lytic EBV replication can contribute greatly to elevations of EBV DNA in plasma, the fractionated quantification of plasma EBV DNA by the methylation assay aids in distinguishing EBV DNA that is tumor-derived from that which is the result of lytic replication. With growing interest in plasma EBV DNA as a serial marker of disease activity in EBV(+) lymphomas, the methylation assay is promising in its ability to differentiate patients with elevated EBV DNA in plasma but ongoing remission from those in whom plasma EBV DNA is tumor-derived and an early harbinger of relapse. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Epigenetic Histone Modification of Epstein-Barr Virus BZLF1 Promoter during Latency and Reactivation in Raji Cells

2012 ◽  
Vol 86 (9) ◽  
pp. 4752-4761 ◽  
Author(s):  
T. Murata ◽  
Y. Kondo ◽  
A. Sugimoto ◽  
D. Kawashima ◽  
S. Saito ◽  
...  
Keyword(s):  
Histone Modification ◽  
Epstein Barr Virus ◽  
Raji Cells ◽  
Barr Virus ◽  
Epstein Barr ◽  
Bzlf1 Promoter

Evidence of lytic infection of Epstein-Barr virus (EBV) in EBV-positive gastric carcinoma

2002 ◽  
Vol 66 (3) ◽  
pp. 351-359 ◽  
Author(s):  
Yoshiko Hoshikawa ◽  
Yukio Satoh ◽  
Masanao Murakami ◽  
Michio Maeta ◽  
Nobuaki Kaibara ◽  
...  
Keyword(s):  
Gastric Carcinoma ◽  
Epstein Barr Virus ◽  
Lytic Infection ◽  
Barr Virus ◽  
Epstein Barr
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