An adult owl monkey (Aotus tricirgatus) used for immunologic studies of Herpesvirus saimiri (HVS) developed early, late, membrane, and neutralizing antibodies to HVS approximately 3 weeks after the beginning of the experiment. HVS was isolated by the cocultivation of peripheral blood for over 1 year. No clinical, gross, or histopathologic findings of malignancy were exhibited by the animal. The HVS isolate from the animal was indistinguishable biologically and serologically from the original HVS strain of Meléndez and from an isolate of an experimentally HVS-induced tumor. Inoculation of this isolate into 2 young white-lipped marmosets (Saguinus fuscicollis) produced typical malignant lymphoma and lymphocytic leukemia. Our findings suggested that the virus from the chronically infected animal was oncogenic and that host factors were primarily responsible for determining the disease manifestation of the virus infection. Another owl monkey chronically infected with HVS for over 2 years has remained asymptomatic.

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).

Lymphoblastoid cells were cultured from twoHerpesvirus saimiri (HVS) inoculated white-lipped marmosets and from one HVS-inoculated owl monkey. Cells from all three animals grew clumped in suspension. The cells from both species were diploid in chromo-some number and showed no unusual chromosomal abnormalities. The marmoset cell line examined was chimaeric. The marmoset cells lacked HSV-associated antigens as determined by immunofluorescence, and no evidence for the presence of virus was found by either infectivity assays or electron microscopy. Cocultivation of these cells with Vero cells resulted in cytopathology and the recovery of complete, infectious virus. The owl monkey lymphoid cells were positive to a small degree for both viral antigens and infectivity. The cells were resistant to rechallenge with HVS. Cocultivation of these cells with Vero cells led to the development of cytopathology and an increased yield of virus.

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

Summary Herpesvirus saimiri (HVS)-induced intracellular and cell membrane antigens were demonstrated in infected owl monkey cells by indirect immunofluorescence methods. Sera from HVS-infected owl monkeys were the source of antibody. The fluorescent reagent was a fluorescein isothiocyanate (FITC)-conjugated caprine antihuman γ-globulin. The effectiveness of the procedure was evaluated on owl-monkey lymphoid cells infected with HVS. Intracellular antigens were detected in infected cells after in vitro cultivation but not in uninfected cells or fresh biopsy material from HVS-infected monkeys. These antigens were demonstrated with post-HVS infection sera from 6 owl monkeys but not with sera taken before or within 5 days after HVS infection. HVS-associated membrane antigens were shown in cells productively infected with the virus. The appearance of these antigens coincided with cytopathogenic changes associated with the viral infection. This was particularly evident in an infected owl-monkey kidney culture where only the rounded cells, not the adherent monolayer, contained both intracellular and membrane antigens. Similar observations were obtained when vero cells, cocultivated with a non-virus-producing marmoset lymphoid cell line, showed cytopathology characteristic of HVS infection. These results demonstrate that membrane antigens are expressed in cells infected with HVS and suggest that their synthesis is a late event in the replicative cycle of this virus.