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Correspondence |
University of Zurich Zurich, Switzerland
Swiss Paraplegic Centre Nottwil, Switzerland
To the Editor-in-Chief:
With special interest we studied the article titled, "A Defective, Rearranged Epstein-Barr Virus Genome in EBER-Negative and EBER-Positive Hodgkin’s Disease," by Gan and colleagues,1 published in the March 2002 issue of The American Journal of Pathology. The authors assessed the presence of the BamHI W/Z rearrangement, known to disrupt viral latency,2 in clinical samples of 56 American and Brazilian children and adolescents suffering from Hodgkin’s disease (HD). Applying a sensitive PCR assay on DNA extracted from paraffin-embedded material, Gan et al1 detected the juxtaposition of the BamHI W and Z fragments in 10 of 32 (31%) EBER-positive and in 8 of 24 EBER-negative HD tumors.
In 1992, we addressed this issue with a sensitive PCR detection system for the BamHI W/Z rearrangement in EBV-positive HD.3 Genomic DNA was purified under sterile conditions from fresh frozen lymph node biopsies of 21 adult Swiss patients. Sixteen patients suffered from EBV-positive HD (LMP1 expressing Reed-Sternberg cells) and five from EBV-associated angioimmunoblastic lymphadenopathy. All biopsy samples contained a high number of EBV-copies, in particular 15 samples ≥104 copies per 1 µg DNA and six samples with 103 copies per 1 µg DNA, when tested with a semi-quantitative graduated dilution method.4 The cell line P3J-HR-1, clone HH543–5 (a kind gift from Dr. G. Miller, Yale University), was used as a positive control for BamHI W/Z rearrangements.3 The results were verified by Southern blotting with subsequent specific hybridization including the positive control.
In comparing our findings in EBV-positive HD (all 16 HD cases negative for BamHI W/Z rearrangements) with the results of Gan and colleagues1 (32% positive), it should be noted that this significant difference occurred even though both groups used a very sensitive PCR detection method; and samples with a high EBV-copy number. What then could make up for this difference? Could it be the geographic origin of the samples? We don’t think so, because another polymorphism within the EBV genome, the 30-bp LMP1-deletion variant, is observed at equal frequency (59 to 75%) in infectious mononucleosis or EBV-associated tonsillar hyperplasia of children and adolescents from Brazil, North America, and Switzerland.5,6
What remains, therefore, is the difference of age at diagnosis of HD, which was 40 years (mean) in our series. In adults, a putative loss of defective EBV genomes harboring BamHV W/Z rearrangements over time might be a consequence of a still immunocompetent organism in childhood and early adulthood, and in the years before development of HD which is associated with impaired T-cell immunity.7
References
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