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Journal of Clinical Microbiology, June 2000, p. 2458-2458, Vol. 38, No. 6
0095-1137/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
LETTERS TO THE EDITOR
No Correlation in Epstein-Barr Virus Reactivation Between
Serological Parameters and Viral Load
 |
LETTER |
Epstein-Barr virus (EBV) has been identified as a cofactor in the
pathogenesis of a significant proportion of human immunodeficiency virus (HIV)-related or transplantation-related lymphoproliferative disorders (2, 3). Furthermore, EBV reactivation occurs more frequently in patients on hemodialysis due to the uremic
immunodeficiency (5). Currently, EBV reactivations are
almost exclusively diagnosed by antibody assays. We investigated
whether the indirect detection of EBV by serological assays is
correlated with the direct detection of the EBV viral DNA load in
patients with immunosuppression (30 HIV-positive individuals, 30 transplant recipients, 23 patients on hemodialysis) and in 30 blood
donors as controls. EBV primary infections and seronegatives were excluded.
First, immunofluorescence analysis of immunoglobulin G (IgG), IgM, and
IgA antibodies to virus-capsid antigen (VCA), early antigen (EA-IgG),
and EBV nuclear antigens 1 and 2 (EBNA1-IgG and EBNA2-IgG,
respectively) were carried out. Serological reactivations were detected
when at least one of the following parameters was found: VCA-IgM titer,
>32; VCA-IgA titer, >32, EA-IgG titer, >64; EBNA1-IgG 
EBNA2-IgG (5).
EBV DNA present in peripheral leukocytes was quantified by a
competitive nested PCR assay of EBV-p23 (1). The detection limit was determined as 20 EBV copies in 105 EBV-negative
leukocytes. In the latent stage, not more than 5 cells in
106 leukocytes are EBV infected; thus, latent infections
were not detectable with this PCR (4).
Serological reactivation and EBV DNA content were not correlated, since
serological reactivations were found with almost the same frequency in
PCR-positive as in PCR-negative individuals (Table
1). No PCR-positive subjects were
present in controls; however, 13% exhibited serological markers for
reactivation. Furthermore, no differences were found when single
serological reactivation parameters such as EA-IgG or EBNA1-IgG EBNA2-IgG were correlated with PCR. Finally, PCR results failed to
correlate with the number of different reactivation markers in
individual subjects. Four patients with a high viral load
(>106 copies/µg of DNA) were found in the group of
PCR-positive subjects. Even among these patients, no serological
reactivations were detected. In contrast, 4 of 11 patients (36%) with
moderate (104 to 106 copies/µg of DNA) and 6 of 7 patients (85%) with low viral load (<104 copies/µg
of DNA) showed such serological reactivations, suggesting that antibody
production and the loss of antibodies are individually different,
particularly in immunosuppressed patients.
In summary, we suggest that the serological parameters that are
currently employed as an indicator for EBV reactivation may be of
limited use as they fail to correlate with viral load.
| |
FOOTNOTES |
*
Phone: 49-6841-163931
Fax: 49-6841-163980
E-mail: vinmue{at}med-rz.uni-sb.de
| |
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| | | | |
Barbara Christine Gärtner
Kerstin Kortmann
Marco Schäfer
Nikolaus Mueller-Lantzsch*
Department of Virology
University of the Saarland
Homburg/Saar, Germany
|
| | | | |
Urban Sester
Harald Kaul
Department of Nephrology
University of the Saarland
Homburg/Saar, Germany
|
| | | | |
Hanns Pees
Department of Hematology and Oncology
University of the Saarland
Homburg/Saar, Germany
|
Journal of Clinical Microbiology, June 2000, p. 2458-2458, Vol. 38, No. 6
0095-1137/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
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