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Full Text Article:
http://www.plosone.org/article/info:doi/10.1371/journal.pone.0085387
Deficient EBV-Specific B- and T-Cell Response in Patients with Chronic Fatigue Syndrome
Madlen Loebel equal contributor *, Kristin Strohschein equal contributor, Carolin Giannini, Uwe Koelsch, Sandra Bauer, Cornelia Doebis, Sybill Thomas, Nadine Unterwalder, Volker von Baehr, Petra Reinke, Michael Knops, Leif G. Hanitsch, Christian Meisel, Hans-Dieter Volk, Carmen Scheibenbogen
Published: January 15, 2014
DOI: 10.1371/journal.pone.0085387
Abstract
Epstein-Barr virus (EBV) has long been discussed as a possible cause or trigger of Chronic Fatigue Syndrome (CFS).
In a subset of patients the disease starts with infectious mononucleosis and both enhanced anddiminished EBV-specific antibody titers have been reported.
In this study, we comprehensively analyzed the EBV-specific memory B- and T-cell response in patients with CFS. While we observed no difference in viral capsid antigen (VCA)-IgG antibodies, EBV nuclear antigen (EBNA)-IgG titers were low or absent in 10% of CFS patients.
Remarkably, when analyzing the EBV-specific memory B-cell reservoir in vitro a diminished or absent number of EBNA-1- and VCA-antibody secreting cells was found in up to 76% of patients.
Moreover, the ex vivo EBV-induced secretion of TNF-α and IFN-γ was significantly lower in patients. Multicolor flow cytometry revealed that the frequencies of EBNA-1-specific triple TNF-α/IFN-γ/IL-2 producing CD4+ and CD8+T-cell subsets were significantly diminished whereas no difference could be detected for HCMV-specific T-cell responses.
When comparing EBV load in blood immune cells, we found more frequently EBER-DNA but not BZLF-1 RNA in CFS patients compared to healthy controls suggesting more frequent latent replication.
Taken together, our findings give evidence for a deficient EBV-specific B- and T-cell memory response inCFS patients and suggest an impaired ability to control early steps of EBV reactivation.
In addition the diminished EBV response might be suitable to develop diagnostic marker in CFS.
Eco
http://www.plosone.org/article/info:doi/10.1371/journal.pone.0085387
Deficient EBV-Specific B- and T-Cell Response in Patients with Chronic Fatigue Syndrome
Madlen Loebel equal contributor *, Kristin Strohschein equal contributor, Carolin Giannini, Uwe Koelsch, Sandra Bauer, Cornelia Doebis, Sybill Thomas, Nadine Unterwalder, Volker von Baehr, Petra Reinke, Michael Knops, Leif G. Hanitsch, Christian Meisel, Hans-Dieter Volk, Carmen Scheibenbogen
Published: January 15, 2014
DOI: 10.1371/journal.pone.0085387
Abstract
Epstein-Barr virus (EBV) has long been discussed as a possible cause or trigger of Chronic Fatigue Syndrome (CFS).
In a subset of patients the disease starts with infectious mononucleosis and both enhanced anddiminished EBV-specific antibody titers have been reported.
In this study, we comprehensively analyzed the EBV-specific memory B- and T-cell response in patients with CFS. While we observed no difference in viral capsid antigen (VCA)-IgG antibodies, EBV nuclear antigen (EBNA)-IgG titers were low or absent in 10% of CFS patients.
Remarkably, when analyzing the EBV-specific memory B-cell reservoir in vitro a diminished or absent number of EBNA-1- and VCA-antibody secreting cells was found in up to 76% of patients.
Moreover, the ex vivo EBV-induced secretion of TNF-α and IFN-γ was significantly lower in patients. Multicolor flow cytometry revealed that the frequencies of EBNA-1-specific triple TNF-α/IFN-γ/IL-2 producing CD4+ and CD8+T-cell subsets were significantly diminished whereas no difference could be detected for HCMV-specific T-cell responses.
When comparing EBV load in blood immune cells, we found more frequently EBER-DNA but not BZLF-1 RNA in CFS patients compared to healthy controls suggesting more frequent latent replication.
Taken together, our findings give evidence for a deficient EBV-specific B- and T-cell memory response inCFS patients and suggest an impaired ability to control early steps of EBV reactivation.
In addition the diminished EBV response might be suitable to develop diagnostic marker in CFS.
Eco