CD3-negative lymphoproliferative disease of granular lymphocytes containing Epstein-Barr viral DNA.

K Kawa-Ha; S Ishihara; T Ninomiya; K Yumura-Yagi; J Hara; F Murayama; A Tawa; K Hirai

doi:10.1172/JCI114168

Department of Pediatrics, Osaka University Hospital, Japan.

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Department of Pediatrics, Osaka University Hospital, Japan.

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Department of Pediatrics, Osaka University Hospital, Japan.

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Department of Pediatrics, Osaka University Hospital, Japan.

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Department of Pediatrics, Osaka University Hospital, Japan.

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Department of Pediatrics, Osaka University Hospital, Japan.

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Published in Volume 84, Issue 1 on July 1, 1989
J Clin Invest. 1989;84(1):51–55. https://doi.org/10.1172/JCI114168.
© 1989 The American Society for Clinical Investigation

Published July 1, 1989 - Version history

Lymphoproliferative disease of granular lymphocytes (LDGL) is a heterogeneous disorder and the pathogenesis is likely to be complex. Some patients with chronic active EBV (CAEBV) infection also have LDGL. To investigate the relationship between EBV infection and the pathogenesis of LDGL, we conducted a survey for EBV DNA sequences by Southern blot analysis of DNA obtained from the peripheral blood of seven patients with LDGL, including one with CAEBV infection. Interestingly, EBV DNA was detected in the sample from the patient with CAEBV infection, and in the samples from four other patients with CD3-LDGL. Moreover, a single band for the joined termini of the EBV genome was demonstrated in two samples, suggesting a clonal disorder of those LDGL. These findings strongly suggest that EBV may play a pathogenic role in some cases of LDGL.

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