virus (EBV) titers were measured in the sera of 37 patients with Hodgkin's disease and ia 40 normal controls. The patients were grouped according to histologic type, clinical symptomatology (relapse or remission), and their immune state (immunodeficient or non-immanodeficient). AntiEpstein-Barr nuclear antigens (EBNA) and antiviral capside antigens (VGA) titers were higher in patients with Hodgkin's disease than in the controls. Anti-EBNA titers were significantly higher in patients with lymphocyte predominance, and anti-VCA titers were significantly higher itl patients with mixed cellularity. Patients in clinical relapse had higher anti-EBV antibody titers than patients in remission or those in the control group. Immunodeficient patients had significantly higher anti-VCA titers than either the non-immunodeficient or the control cases. We believe high anti-EBV titers are related to immunodeficiencies. The relationship between Hodgkin's disease and EBV is discussed.

A total of 122 sera from acute lymphoblastic leukemia (ALL) patients were analyzed for circulating immune complexes (CIC) by two methods: the 125I-Clq binding assay and the polyethylene glycol precipitation test (PEG). The results were correlated with induction, remission and relapse stages of the disease. Using the first method the levels of CIC in induction were 15.18 +/- 9.15, with 19/29 positive cases (65.50%), P less than 0.001 compared with controls. In the remission phase the levels were 9.02 +/- 5.62, 11/45 (24.49%) nonsignificant P value, and in relapse they were 16.14 +/- 11.17 28/48 (58.33%) P less than 0.001. The PEG precipitation test results were: 0.33 +/- 0.10, 8/22 (36.36%); 0.24 +/- 0.11, 10/48 (20.83%) and 0.28 +/- 0.10, 6/28 (21.42%), respectively. Thus the values of CIC as measured by PEG in the three clinical of phases ALL did not differ significantly from controls. This contrasts with results obtained by the radioiodinated C1q binding assay, where the incidence of positive values was significantly higher in induction and in relapse and lower in the remission phase. These observations were extended in sequential vertical studies performed in a group of patients. These results suggest that raised CIC detected by the 125I-C1q method may reflect a progressive state in ALL and that quantitation of these immune complexes may provide an adequate biochemical marker for prognosis.

Murine lymphoid chalones and their in vivo effect were studied. Cytoplasmic extracts were prepared from normal murine spleen lymphocytes. When assayed in vitro, cytoplasmic extracts (CE) were able to inhibit a blastomitogenic phytohemagglutinin (PHA) response of syngeneic and allogeneic normal murine lymphocytes, as well as cell replication of murine lymphoma cells. CE also had an inhibitory effect on human lymphoblastoid cell line division but it had no effect on nonlymphoid cell division. In vivo, CE had an enhancing effect on a murine allogeneic tumor, probably by suppressing the host’s immune rejection response.