A 58-year-old Chinese man presented initially with generalized lymphadenopathy, and lymph-node biopsy showed disturbed architecture with preponderance of large B-blasts mixed with numerous CD8+ T lymphocytes, consistent with an acute Epstein-Barr virus(EBV) infection, lmmunohistological and gene rearrangement studies confirmed the absence of clonal T or B cells. Polyclonal EBV with lytic infection was detected by Southern blot hybridization (SoBH). Expression of EBV proteins (EBNA2. LMP and ZEBRA) was detected in a proportion of cells by immunostaining. EBV-lytic proteins โฌA-D, VCA. MA were also detected in rare scattered cells. Double immunostaining showed that the LMP-positive cells were of B and of T phenotype: 73% CDI9+, 26% C02+. 23% CD3+, 8% CD4-. 17% CD8+. After biopsy, there was spontaneous regression of lymph-node enlargement, but lymphadenopathy recurred 8 months later, and the second lymph-node biopsy showed T-cell lymphoma, confirmed by detection of clonally rearranged T-cellreceptor beta-chain gene. However, EBV genome could not be detected in the second biopsy by SoBH, in situ hybridization for EBV-encoded EBER RNA, and immunostaining for EBNA2, LMP and ZEBRA was also negative. This case is of special interest because an EBV-negative T-cell lymphoma developed shortly after an acute episode of EBV-related lymphoproliferation, even though many EBV-positive T cells were detected during the acute episode. EBV was apparently not a direct cause of the lymphoma, but the close temporal association of the 2 lesions supports the hypothesis that EBV can act as a co-factor in lymphomagenesis. 1 1994 lvll~~-l,l\, I t K .