Dynamics of Epstein‐Barr virus DNA levels in serum during EBV‐associated disease

Berger, Christoph; Day, Philip J.; Meier, Gabriela; Zingg, Walter; Bossart, Walter; Nadal, David

doi:10.1002/jmv.1078.abs

Cited by 34 publications

(66 citation statements)

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“…This high prevalence increased to 59% if the analysis was limited to pleural effusions where the nature of the effusion was unclear. These real-time PCR data were confirmed by a different PCR assay targeting another region of the EBV genome [15], (results not shown). …”

Section: Discussionmentioning

confidence: 66%

A possible role for Epstein-Barr virus in the pathogenesis of pleural effusion

Thijsen¹

2005

European Respiratory Journal

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A high percentage of pleural effusions remain unexplained despite an intensive diagnostic workup. Epstein-Barr virus (EBV) infections occur worldwide and affect the majority of the population. The present study investigated the prevalence and clinical relevance of EBV in pleural effusions.A prospective study was performed in which 60 consecutive patients with pleural effusion were enrolled. Real-time quantitative EBV-PCR was performed on pleural fluid and serum. Pleural fluid was further evaluated using standard biochemical, cytological and microbiological procedures. Demographic data, medical history and medication were recorded.A total of 24 (40%), from 60 pleural fluids tested, were positive in the EBV-PCR. Median EBV-DNA levels for positive samples was 454 genome equivalents (geq)?mL -1 (range 36-163,446 geq?mL -1 ). A total of 20 (59%) out of 34 unexplained pleural effusions were EBV-PCR positive.Serological analysis of all patients with a positive PCR revealed a previous infection. Patients with a positive EBV-PCR on pleural fluid were more likely to have a positive EBV-PCR on serum than patients with a negative PCR on pleural fluid. Epstein-Barr virus reactivation in pleural fluid is a frequent event and the absence of an alternative diagnosis to explain the nature of the effusion in the majority of cases suggests an aetiological role for Epstein-Barr virus in the development of pleural effusion.

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Section: Discussionmentioning

confidence: 66%

A possible role for Epstein-Barr virus in the pathogenesis of pleural effusion

Thijsen¹

2005

European Respiratory Journal

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“…DNA extraction from intact virus and qPCR for the EBV conserved BamHI W region was performed as described (Berger et al, 2001).…”

Section: Methodsmentioning

confidence: 99%

TLR9 triggering in Burkitt's lymphoma cell lines suppresses the EBV BZLF1 transcription via histone modification

et al. 2010

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Endemic Burkitt's lymphoma (BL) is considered to preferentially develop in equatorial Africa because of chronic co-infection with Epstein-Barr virus (EBV) and the malaria pathogen Plasmodium falciparum. The interaction and contribution of both pathogens in the oncogenic process are poorly understood. Earlier, we showed that immune activation with a synthetic Toll-like receptor 9 (TLR9) ligand suppresses the initiation of EBV lytic replication in primary human B cells. In this study we investigate the mechanism involved in the suppression of EBV lytic gene expression in BL cell lines. We show that this suppression is dependent on functional TLR9 and MyD88 signaling but independent of downstream signaling elements, including phosphatidylinositol-3 kinase, mitogen-activated protein kinases and nuclear factor-jB. We identified TLR9 triggering resulting in histone modifications to negatively affect the activation of the promoter of EBV's master regulatory lytic gene BZLF1. Finally, we show that P. falciparum hemozoin, a natural TLR9 ligand, suppresses induction of EBV lytic gene expression in a dose-dependent manner. Thus, we provide evidence for a possible interaction between P. falciparum and EBV at the B-cell level and the mechanism involved in suppressing lytic and thereby reinforcing latent EBV that has unique oncogenic potential.

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“…EBV DNA can therefore be determined in serum or plasma as well as in PBMCs [84] . In patients with primary infection, it is frequently detected in whole blood (PBMCs and plasma/serum) within 14 d of symptom onset [85][86][87][88][89] . After the initiation of an immune response, viral load decreases slowly in PBMCs, but rapidly in plasma/serum, and it becomes undetectable after 3-4 wk [90][91][92] , whereas memory cells with EBV may remain latent for a long time in blood.…”

Section: Molecular Biologymentioning

confidence: 99%

Serological diagnosis of Epstein-Barr virus infection: Problems and solutions

Paschale

Clerici²

2012

WJV

242

257

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Serological tests for antibodies specific for Epstein-Barr virus (EBV) antigens are frequently used to define infection status and for the differential diagnosis of other pathogens responsible for mononucleosis syndrome. Using only three parameters [viral capsid antigen (VCA) IgG, VCA IgM and EBV nuclear antigen (EBNA)-1 IgG],it is normally possible to distinguish acute from past infection: the presence of VCA IgM and VCA IgG without EBNA-1 IgG indicates acute infection, whereas the presence of VCA IgG and EBNA-1 IgG without VCA IgM is typical of past infection. However, serological findings may sometimes be difficult to interpret as VCA IgG can be present without VCA IgM or EBNA-1 IgG in cases of acute or past infection, or all the three parameters may be detected simultaneously in the case of recent infection or during the course of reactivation. A profile of isolated EBNA-1 IgG may also create some doubts. In order to interpret these patterns correctly, it is necessary to determine IgG avidity, identify anti-EBV IgG and IgM antibodies by immunoblotting, and look for heterophile antibodies, anti-EA (D) antibodies or viral genome using molecular biology methods. These tests make it possible to define the status of the infection and solve any problems that may arise in routine laboratory practice.

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Dynamics of Epstein‐Barr virus DNA levels in serum during EBV‐associated disease

Cited by 34 publications

References 0 publications

A possible role for Epstein-Barr virus in the pathogenesis of pleural effusion

A possible role for Epstein-Barr virus in the pathogenesis of pleural effusion

TLR9 triggering in Burkitt's lymphoma cell lines suppresses the EBV BZLF1 transcription via histone modification

Serological diagnosis of Epstein-Barr virus infection: Problems and solutions

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