Heterogeneous Epstein–Barr virus latent gene expression in AIDS-associated lymphomas and in type I Burkitt's lymphoma cell lines

Robert, Thomas; Arbach, Hratch; Cochet, C; Feuillard, Jean; Martin, Antoine; Raphaël, Martine; Joab, Irène

doi:10.1099/vir.0.18687-0

Cited by 16 publications

(7 citation statements)

References 20 publications

(13 reference statements)

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“…One possible connection between stress and cancer development is the reactivation of latent tumor promoting viruses. As already discussed, EBV is associated with NPC, BL, nonHodgkin_s lymphoma, and posttransplant lymphomas (Ansell et al 1999;Brousset 2002;Petrella et al 1997;Touitou et al 2003). Because stress can promote latent virus reactivation, it is plausible that there is a relationship between stress and EBV-associated tumors.…”

Section: Cancermentioning

confidence: 93%

“…EBV is a gamma herpesvirus and the etiological agent for infectious mononucleosis, and is a human tumor virus implicated in several malignant diseases including nasopharyngeal carcinoma (NPC), African Burkitt_s lymphoma (BL), B cell lymphoma, and posttransplant lymphomas (Ansell et al 1999;Brousset 2002;Petrella et al 1997;Touitou et al 2003). Several studies have demonstrated that stress promotes latent EBV reactivation, which is reflected in the higher antibody titers to EBV antigens such as the virus capsid antigen (VCA).…”

Section: Latent Virus Reactivationmentioning

confidence: 98%

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Stress-Induced Immune Dysregulation: Implications for Wound Healing, Infectious Disease and Cancer

Godbout

Glaser

2006

Jrnl Neuroimmune Pharm

328

224

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The communication between the central nervous system and the immune system occurs via a complex network of bidirectional signals linking the nervous, endocrine and immune systems. The field of psychoneuroimmunology (PNI) has provided new insights to help understand the pathophysiological processes that are linked to the immune system. Work in this field has established that psychological stress disrupts the functional interaction between the nervous and immune systems. Stress-induced immune dysregulation has been shown to be significant enough to result in health consequences, including reducing the immune response to vaccines, slowing wound healing, reactivating latent herpesviruses, such as Epstein-Barr virus (EBV), and enhancing the risk for more severe infectious disease. Chronic stress/depression can increase the peripheral production of proinflammatory cytokines, such as interleukin (IL)-6. High serum levels of IL-6 have been linked to risks for several conditions, such as cardiovascular disease, type 2 diabetes, mental health complications, and some cancers. This overview will discuss the evidence that psychological stress promotes immune dysfunction that negatively impacts human health.

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Section: Cancermentioning

confidence: 93%

Section: Latent Virus Reactivationmentioning

confidence: 98%

Stress-Induced Immune Dysregulation: Implications for Wound Healing, Infectious Disease and Cancer

Godbout

Glaser

2006

Jrnl Neuroimmune Pharm

328

224

View full text Add to dashboard Cite

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“…Indeed, related transcripts (using the lytic Fp immediately upstream of Qp) have been found in latency I BL cell lines induced to enter the lytic cycle (Touitou et al 2003). Additionally, a subset of BLs that carry a deletion of EBNA2 express the EBNA3s from the Wp promoter (Kelly et al 2002).…”

Section: Ebna3s In B Cell Lymphomagenesismentioning

confidence: 98%

The EBNA3 Family: Two Oncoproteins and a Tumour Suppressor that Are Central to the Biology of EBV in B Cells

Allday

Bazot

White

2015

Current Topics in Microbiology and Immunology

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Epstein-Barr virus nuclear antigens EBNA3A , EBNA3B and EBNA3C are a family of three large latency-associated proteins expressed in B cells induced to proliferate by the virus. Together with the other nuclear antigens (EBNA-LP, EBNA2 and EBNA1), they are expressed from a polycistronic transcription unit that is probably unique to B cells. However, compared with the other EBNAs, hitherto the EBNA3 proteins were relatively neglected and their roles in EBV biology rather poorly understood. In recent years, powerful new technologies have been used to show that these proteins are central to the latency of EBV in B cells, playing major roles in reprogramming the expression of host genes affecting cell proliferation, survival, differentiation and immune surveillance. This indicates that the EBNA3s are critical in EBV persistence in the B cell system and in modulating B cell lymphomagenesis. EBNA3A and EBNA3C are necessary for the efficient proliferation of EBV-infected B cells because they target important tumour suppressor pathways--so operationally they are considered oncoproteins. In contrast, it is emerging that EBNA3B restrains the oncogenic capacity of EBV, so it can be considered a tumour suppressor--to our knowledge the first to be described in a tumour virus. Here, we provide a general overview of the EBNA3 genes and proteins. In particular, we describe recent research that has highlighted the complexity of their functional interactions with each other, with specific sites on the human genome and with the molecular machinery that controls transcription and epigenetic states of diverse host genes.

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“…Clinical specimens from patients with the diagnosis of BL have been found to express a heterogeneous latency program (25)(26)(27). The heterogeneity of EBV latency patterns in clinical specimens may be due to variant EBV clones, the establishment of immunoprivileged sites in the tumor microenvironment, and the selection of a clone from a type III progenitor pool (23,28).…”

Section: Discussionmentioning

confidence: 99%

EBV MicroRNAs in Primary Lymphomas and Targeting of CXCL-11 by ebv-mir-BHRF1-3

et al. 2008

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EBV-encoded microRNAs (miRNAs) have been identified and their functions are being studied. The expression pattern of these miRNAs in clinical samples of EBV-associated nonHodgkin's lymphomas is unknown. We analyzed five primary ''endemic'' pediatric Burkitt's lymphomas (BL), two acquired immunodeficiency syndrome (AIDS)-related type I latency BL lines, a type III latency line, three EBV + primary effusion lymphomas (PEL), and three AIDS-related diffuse large B-cell lymphomas (DLBCL) for expression of EBV-encoded miRNAs.

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Heterogeneous Epstein–Barr virus latent gene expression in AIDS-associated lymphomas and in type I Burkitt's lymphoma cell lines

Cited by 16 publications

References 20 publications

Stress-Induced Immune Dysregulation: Implications for Wound Healing, Infectious Disease and Cancer

Stress-Induced Immune Dysregulation: Implications for Wound Healing, Infectious Disease and Cancer

The EBNA3 Family: Two Oncoproteins and a Tumour Suppressor that Are Central to the Biology of EBV in B Cells

EBV MicroRNAs in Primary Lymphomas and Targeting of CXCL-11 by ebv-mir-BHRF1-3

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