Antibody-dependent lymphocyte cytotoxicity (ADLC) was demonstrated against Epstein-Barr virus (EBV)-infected RAJI cells with peripheral with peripheral blood lymphocytes from EBV-infected donors. No cytotoxic activity was detected against unifected RAJl cells. The results indicated that this antibody-mediated cytotoxic reaction was directed against the same EBV-induced membrane antigens (MA) previously defined by the membrane immunofluorescence (MF) assay. Antibody to EBV-associated early antigens did not participate in this in vitro reaction. Antibody titers to EBV-induced MA were significantly higher by the ADLC assay in comparison with the MF test. A preliminary study showed no relationship between high antibody titers and the presence of EBV-associated malignancies. The possible in vivo significance of this immune reaction was discussed.

Two cases of lymphoma and one case of lymphoproliferative disease were found in a group of 7 owl monkeys imported into our colony as a single group. Herpesvirus saimiri (HVS) was isolated from the tumor cells of 1 lymphoma by cocultivation and from kidney cell cultures from the monkey with lymphoproliferative disease. Antibody to HVS was found in serum samples from 2 monkeys positive for HVS but not in the sera from the 4 clinically normal monkeys. Antibody to Epstein-Barr virus-infected cells was also found in the serum from the animal with lymphoma.

Herpesvirus saimiri (HVS) induced persistent, clinically inapparent infections of long-term duration in capuchin monkeys (Cebus albifrons). The infections were characterized by development of antibody to HVS-associated antigens and recovery of low levels of virus-genome-carrying lymphocytes in the peripheral blood. Peripheral lymphocyte counts remained in low-normal to normal ranges and no physical signs of lymphoma were evident. Prednisolone treatment caused immunosuppression in one monkey; this was accompanied by a progressive loss of humoral antibody to HVS-associated antigens, but neoplastic disease did not develop.

The association between the induction of antibodies to early antigens (EA) with the detection of virusinfected peripheral blood lymphocytes, and the possible correlation of these factors with the response of lymphocytes to different mitogens was investigated in owl monkeys infected with Herpesvirus saimiri (HVS). There was a positive correlation between the production of antibodies to EA and the quantitative recovery of virus from peripheral blood lymphocytes. The loss of responsiveness of lymphocytes from leukemic owl monkeys to T-cell mitogens paralleled these two parameters suggesting that virus genome-carrying lymphocytes are functionally altered.

Antibody-response patterns to 3 major groups of Herpesvirus saimiri (HVS)-associated antigens [early antigens (EA), late antigens (LA), membrane antigens (MA)] in 10 owl monkeys infected with HVS were related to the clinical course of HVS-induced disease. Results are also presented which show that EA is produced 4–8 hours earlier than LA in HVS-infected cells providing further evidence that these were 2 distinct groups of antigens. In animals that developed neoplasms, antibodies against all 3 groups of antigens were found; however, the antibody response to EA was delayed, in general, 2–4 weeks compared with the responses to LA and MA. Two owl monke,s inoculated with HVS and one inoculated with HVS-induced tumor cells did not develop gross or clinical signs of disease; antibodies to LA and MA, but not EA, were detected in serum samples from these monkeys. These results provide additional evidence that the antibody response to EA may indicate lymphoproliferation (or cell transformation).

Journal Article A Continuous In Vitro Source of Herpesvirus saimiri Get access H. K. Oie, H. K. Oie Search for other works by this author on: Oxford Academic PubMed Google Scholar D. V. Ablashi, D. V. Ablashi Search for other works by this author on: Oxford Academic PubMed Google Scholar G. R. Armstrong, G. R. Armstrong Search for other works by this author on: Oxford Academic PubMed Google Scholar G. R. Pearson, G. R. Pearson Search for other works by this author on: Oxford Academic PubMed Google Scholar T. Orr, T. Orr Search for other works by this author on: Oxford Academic PubMed Google Scholar U. Heine U. Heine Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 51, Issue 3, September 1973, Pages 1077–1080, https://doi.org/10.1093/jnci/51.3.1077 Published: 01 September 1973 Article history Received: 22 May 1973 Accepted: 12 June 1973 Published: 01 September 1973