TABLE 1.

Prevalence of SV40 DNA in EBV-immortalized LCLs

Derivation of LCLsa	Source	Mean age (yr) of patient or donor (range)	No. of LCLs with SV40 large-Tag sequences/no. of LCLs examinedb
Obtained by spontaneous outgrowth	NHLc biopsy specimens	72 (66-78)	0/4
	HD biopsy specimens	44 (23-77)	6/8
	Reactive lymphadenopathies	51.5 (35-68)	0/2
	PBMCs of healthy donors	59	1/1
	Total	52.1 (23-78)	7/15 (46.7%)
Induced with the B95.8 EBV strain	PBMCs of HD patients	41.8 (17-77)	9/14
	PBMCs of healthy donors	33.5 (22-50)	6/13
	Total	37.3 (17-77)	15/27 (55.5%)

^aThe LCLs analyzed were established at different times over a 5-year period (1991 to 1996). Spontaneous LCLs were derived from biopsy specimens and PBMCs as previously described (7). Briefly, finely minced fragments from biopsy material were placed in fetal calf serum-coated 24-well plates and cultured in RPMI 1640 medium (GIBCO, Grand Island, N.Y.) supplemented with 10% heat-inactivated fetal calf serum, 2 mmol of l-glutamine/liter, 100 IU of penicillin/ml, and 100 IU of streptomycin/ml (complete medium). Purified PBMCs (10⁶/ml), obtained by Ficoll-Hypaque gradient centrifugation, were seeded in 96-flat-well plates and cultured in 200 μl of complete medium. Cyclosporin A (0.1 μg/ml; Sigma, St. Louis, Mo.) was added to the medium to inhibit T-cell activation. LCLs carrying the B95.8 prototypic EBV strain (B95.8 LCLs) were established by infecting PBMCs from lymphoma patients or healthy donors with spent supernatant of the B95.8 marmoset cell line.

^bIn all, 22 of 42 (52.3%) LCLs contained SV40 large-Tag sequences.

^cNHL, non-Hodgkin's lymphoma.