The etiology of LGL leukemia is not known; however, we recently detect
ed HTLV-II in a patient with LGL leukemia. In this study, we found tha
t sera from 6 of 28 patients with LGL leukemia were positive for HTLV-
I/II using a whole virus ELISA; moreover, the ELISA-negative sera were
near the positive cut-off value. Therefore, we performed additional s
tudies on these sera using commercially available assays which can con
firm and distinguish HTLV-I from HTLV-II infection. Serum from on ly o
ne patient was confirmed positive using conventional criteria (HTLV-II
+). Sera from 25 patients (89%) had indeterminate reactivity on Wester
n blot assays. Of these, sera from 21 (84%) reacted to gag protein p24
; 12 (48%) reacted with recombinant env protein p21e, and 10 (40%) rea
cted with both. We could not detect HTLV-I/ II pol or pX gene sequence
s in these patients using polymerase chain reaction analyses, with the
exception of the HTLV-II-infected patient described previously. These
data show that most patients with LGL leukemia are not infected with
prototypical HTLV-I or HTLV-II. The frequent reactivity of patient ser
a to HTLV-I/II gag protein p24 and to env protein p21e, however, sugge
sts that a deleted or variant farm of HTLV-I/II may be associated with
LGL leukemia.