scholarly journals Activation of Epstein-Barr virus replication in Hodgkin and Reed- Sternberg cells

Blood ◽  
1991 ◽  
Vol 78 (5) ◽  
pp. 1162-1165
Author(s):  
G Pallesen ◽  
K Sandvej ◽  
SJ Hamilton-Dutoit ◽  
M Rowe ◽  
LS Young
Keyword(s):  
Epstein Barr Virus ◽  
Viral Latency ◽  
Virus Genome ◽  
Latent Membrane Protein ◽  
Gene Products ◽  
Barr Virus ◽  
Membrane Antigens ◽  
Ebv Dna ◽  
Epstein Barr ◽  
Cryostat Sections

Recent evidence has shown that Hodgkin's disease (HD) is associated with Epstein-Barr virus (EBV) in a substantial number of cases and that in these cases EBV DNA is localized exclusively to Hodgkin and Reed- Sternberg (RS) cells. The virus genome is not silent in RS cells because two EBV latent gene products, latent membrane protein (LMP) and EB early region (EBER) transcripts, have recently been reported to be expressed in RS cells. However, little information is available about the possible activation of EBV replicative genes in HD. This prompted us to investigate HD biopsies from 96 patients for expression of replicative gene products. Cryostat sections were immunostained with monoclonal antibodies to protein BZLF1, which controls the switch between EBV latency and replication, and also to LMP. LMP was demonstrated in RS cells in 47 cases (49%). Three of the LMP-positive cases (6%), but none of the LMP-negative cases, expressed the BZLF1 protein. BZLF1 positively was confined to rare RS cells. These three cases showed no detectable early, virus capsid, or membrane antigens. Our findings show that activation of EBV immediate early genes occurs only infrequently in RS cells, indicating that control of viral latency is not severely impaired in HD patients.

scholarly journals Activation of Epstein-Barr virus replication in Hodgkin and Reed- Sternberg cells

Blood ◽  
1991 ◽  
Vol 78 (5) ◽  
pp. 1162-1165 ◽  
Author(s):  
G Pallesen ◽  
K Sandvej ◽  
SJ Hamilton-Dutoit ◽  
M Rowe ◽  
LS Young
Keyword(s):  
Epstein Barr Virus ◽  
Viral Latency ◽  
Virus Genome ◽  
Latent Membrane Protein ◽  
Gene Products ◽  
Barr Virus ◽  
Membrane Antigens ◽  
Ebv Dna ◽  
Epstein Barr ◽  
Cryostat Sections

Abstract Recent evidence has shown that Hodgkin's disease (HD) is associated with Epstein-Barr virus (EBV) in a substantial number of cases and that in these cases EBV DNA is localized exclusively to Hodgkin and Reed- Sternberg (RS) cells. The virus genome is not silent in RS cells because two EBV latent gene products, latent membrane protein (LMP) and EB early region (EBER) transcripts, have recently been reported to be expressed in RS cells. However, little information is available about the possible activation of EBV replicative genes in HD. This prompted us to investigate HD biopsies from 96 patients for expression of replicative gene products. Cryostat sections were immunostained with monoclonal antibodies to protein BZLF1, which controls the switch between EBV latency and replication, and also to LMP. LMP was demonstrated in RS cells in 47 cases (49%). Three of the LMP-positive cases (6%), but none of the LMP-negative cases, expressed the BZLF1 protein. BZLF1 positively was confined to rare RS cells. These three cases showed no detectable early, virus capsid, or membrane antigens. Our findings show that activation of EBV immediate early genes occurs only infrequently in RS cells, indicating that control of viral latency is not severely impaired in HD patients.

scholarly journals Methylation of the Epstein-Barr Virus Genome in Normal Lymphocytes

Blood ◽  
1997 ◽  
Vol 90 (11) ◽  
pp. 4480-4484 ◽  
Author(s):  
Keith D. Robertson ◽  
Richard F. Ambinder
Keyword(s):  
B Cells ◽  
Epstein Barr Virus ◽  
Defense Mechanism ◽  
Immune Surveillance ◽  
Virus Genome ◽  
Barr Virus ◽  
The Face ◽  
Ebv Dna ◽  
Epstein Barr

Abstract Epstein-Barr virus (EBV) latent infection in B cells persists over years or decades despite a sustained cytotoxic immune response to viral antigens. We present data that methylated EBV DNA can be detected in the normal lymphocytes of healthy volunteers. Whereas methylation of foreign DNA has been recognized as a potential cellular defense mechanism, methylation of EBV DNA may be an essential part of the virus life cycle in vivo, explaining the persistence of virus-infected B cells in the face of immune surveillance. Methylation of the C promoter helps to prevent expression of the immunodominant antigens expressed from this promoter. First recognized in tumors, methylation-associated evasion of immune surveillance is not an aberration restricted to tumor tissue but is detected in normal EBV-infected lymphocytes. Methylation of the viral genome in latency also provides an explanation for the CpG suppression associated with EBV but not other large DNA viruses.

Type 2 Epstein-Barr Virus Genome and Latent Membrane Protein-1 Expression in a T-Cell-Rich Lymphoma of Probable B-Cell Lineage

1993 ◽  
Vol 100 (5) ◽  
pp. 541-549 ◽  
Author(s):  
Riccardo Dolcetti ◽  
Antonino Carbone ◽  
Vittorina Zagonel ◽  
Valli De Re ◽  
Annunziata Gloghini ◽  
...  
Keyword(s):  
Membrane Protein ◽  
B Cell ◽  
Epstein Barr Virus ◽  
Cell Lineage ◽  
Virus Genome ◽  
Latent Membrane Protein ◽  
Latent Membrane Protein 1 ◽  
Barr Virus ◽  
Epstein Barr

Epstein-Barr Virus RNA Detection and Glandular Differentiation in Nasopharyngeal Carcinoma

2000 ◽  
Vol 124 (9) ◽  
pp. 1369-1372
Author(s):  
Dhanpat Jain ◽  
Vinita Parkash ◽  
Maomi Li ◽  
James Gill ◽  
Jill Crouch ◽  
...  
Keyword(s):  
Epstein Barr Virus ◽  
Virus Genome ◽  
Undifferentiated Carcinoma ◽  
Latent Membrane Protein ◽  
Rna Detection ◽  
Barr Virus ◽  
Virus Rna ◽  
Epstein Barr ◽  
Virus Latent Membrane Protein

Abstract Most tumors arising in the nasopharynx are either squamous cell carcinoma or so-called undifferentiated carcinoma of the nasopharyngeal type. Primary adenocarcinomas of the nasopharynx are rare, and glandular differentiation in undifferentiated carcinoma of the nasopharyngeal type has not been reported to date. We report 2 cases of undifferentiated carcinoma of the nasopharyngeal type that show distinct glandular differentiation by light microscopy, histochemistry, immunohistochemistry, and ultrastructure. Both tumors showed equal positivity for Epstein-Barr virus latent membrane protein and in situ hybridization for Epstein-Barr virus genome in the undifferentiated areas of the tumor and those featuring glandular differentiation.

scholarly journals Methylation of the Epstein-Barr Virus Genome in Normal Lymphocytes

Blood ◽  
1997 ◽  
Vol 90 (11) ◽  
pp. 4480-4484 ◽  
Author(s):  
Keith D. Robertson ◽  
Richard F. Ambinder
Keyword(s):  
B Cells ◽  
Epstein Barr Virus ◽  
Defense Mechanism ◽  
Immune Surveillance ◽  
Virus Genome ◽  
Barr Virus ◽  
The Face ◽  
Ebv Dna ◽  
Epstein Barr

Epstein-Barr virus (EBV) latent infection in B cells persists over years or decades despite a sustained cytotoxic immune response to viral antigens. We present data that methylated EBV DNA can be detected in the normal lymphocytes of healthy volunteers. Whereas methylation of foreign DNA has been recognized as a potential cellular defense mechanism, methylation of EBV DNA may be an essential part of the virus life cycle in vivo, explaining the persistence of virus-infected B cells in the face of immune surveillance. Methylation of the C promoter helps to prevent expression of the immunodominant antigens expressed from this promoter. First recognized in tumors, methylation-associated evasion of immune surveillance is not an aberration restricted to tumor tissue but is detected in normal EBV-infected lymphocytes. Methylation of the viral genome in latency also provides an explanation for the CpG suppression associated with EBV but not other large DNA viruses.

scholarly journals Consideration of Epstein-Barr Virus-Encoded Noncoding RNAs EBER1 and EBER2 as a Functional Backup of Viral Oncoprotein Latent Membrane Protein 1

mBio ◽  
2016 ◽  
Vol 7 (1) ◽  
Author(s):  
Kristina M. Herbert ◽  
Genaro Pimienta
Keyword(s):  
Membrane Protein ◽  
Epstein Barr Virus ◽  
Viral Latency ◽  
Noncoding Rnas ◽  
Latent Membrane Protein ◽  
Latent Membrane Protein 1 ◽  
Viral Oncoprotein ◽  
Barr Virus ◽  
Ebv Infection ◽  
Epstein Barr

ABSTRACT The Epstein-Barr virus (EBV)-encoded noncoding RNAs EBER1 and EBER2 are highly abundant through all four latency stages of EBV infection (III-II-I-0) and have been associated with an oncogenic phenotype when expressed in cell lines cultured in vitro . In vivo , EBV-infected B cells derived from freshly isolated lymphocytes show that EBER1/2 deletion does not impair viral latency. Based on published quantitative proteomics data from BJAB cells expressing EBER1 and EBER2, we propose that the EBERs, through their activation of AKT in a B-cell-specific manner, are a functionally redundant backup of latent membrane protein 1 (LMP1)—an essential oncoprotein in EBV-associated malignancies, with a main role in AKT activation. Our proposed model may explain the lack of effect on viral latency establishment in EBER-minus EBV infection.

Epstein–Barr Virus and Cancer

2019 ◽  
Vol 14 (1) ◽  
pp. 29-53 ◽  
Author(s):  
Paul J. Farrell
Keyword(s):  
Small Rnas ◽  
Epstein Barr Virus ◽  
Sequence Variation ◽  
Human Cancer ◽  
Virus Genome ◽  
Gene Products ◽  
Barr Virus ◽  
Viral Genes ◽  
Infected Cells ◽  
Epstein Barr

Epstein–Barr virus (EBV) contributes to about 1.5% of all cases of human cancer worldwide, and viral genes are expressed in the malignant cells. EBV also very efficiently causes the proliferation of infected human B lymphocytes. The functions of the viral proteins and small RNAs that may contribute to EBV-associated cancers are becoming increasingly clear, and a broader understanding of the sequence variation of the virus genome has helped to interpret their roles. The improved understanding of the mechanisms of these cancers means that there are great opportunities for the early diagnosis of treatable stages of EBV-associated cancers and the use of immunotherapy to target EBV-infected cells or overcome immune evasion. There is also scope for preventing disease by immunization and for developing therapeutic agents that target the EBV gene products expressed in the cancers.

Quantitative analysis of circulating cell-free Epstein-Barr virus (EBV) DNA levels in patients with EBV-associated lymphoid malignancies

2000 ◽  
Vol 111 (1) ◽  
pp. 239-246 ◽  
Author(s):  
Kenny I. K. Lei ◽  
Lisa Y.S. Chan ◽  
Wing Y. Chan ◽  
Philip J. Johnson ◽  
Y. M. Dennis Lo
Keyword(s):  
Quantitative Analysis ◽  
Epstein Barr Virus ◽  
Barr Virus ◽  
Lymphoid Malignancies ◽  
Ebv Dna ◽  
Epstein Barr

Association of normal oral mucosa with DNA of the main types of oncogenic viruses

2020 ◽  
pp. 60-63
Author(s):  
S.I. Kutukova ◽  
A.B. Chukhlovin ◽  
A.I. Yaremenko ◽  
Yu.V. Ivaskova ◽  
A.Ya. Razumova ◽  
...  
Keyword(s):  
Oral Mucosa ◽  
Epstein Barr Virus ◽  
Oncogenic Viruses ◽  
Viral Dna ◽  
Dna Viruses ◽  
Normal Oral Mucosa ◽  
Barr Virus ◽  
Ebv Dna ◽  
Epstein Barr ◽  
Hpv 18

The aim of the study was to assess the prevalence of DNA viruses (HSV I and II, CMV, EBV, HPV6.11, HPV16 and HPV18) in the native oral mucosa of healthy volunteers (n=50; 30 men (60.0%), 20 women (40.0%); 25—74 years, median age — 55.0 years (95% CI 47.60-56.76)). All samples of the normal oral mucosa were detected by real-time PCR to detect viral DNA. The majority of the examined — 76% (33/50) — revealed the DNA: one type of viral DNA in 17 (38.00%) of the examined, a combination of the two types in 14 (28.00%). In the normal oral mucosa, DNA of Epstein-Barr virus was significantly more often detected: 15 (30.00%) (p = 0.0276) and human papilloma viruses 27 (54.00%) (p <0.0001), especially HPV-18 (24 (48.00%)): mono-association in 9 (18.00%) examined and in 7 (14.00%) in combination with EBV DNA (p = 0.0253).

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