Antiviral cell-mediated immune responses and effect of chromosome polymorphism in Herpesvirus saimiri-infected monkeys.

Herpesvirus saimiri is a horizontally transmitted virus of squirrel monkeys (Saimiri sciureus) which, when inoculated into owl monkeys (Aotus trivirgatus), induces fatal malignant lymphoma in 75 to 80% of the animals. Previous immunological and virological studies have not indicated why 20 to 25% of inoculated owl monkeys develop a chronic, disease-free H. saimiri infection. In the present study, we examined two parameters to explain why certain owl monkeys are resistant to H. saimiri-induced disease. The first possibility was that the animals in which H. saimiri established a chronic infection were all of the same karyotypic class. In studying four such animals, we found that three of the seven known karyotyes were represented, indicating that chromosome polymorphism does not explain disease resistance. The second possibility examined was that animals which develop disease do so as a result of a failure in specific anti-H. saimiri cell-mediated immunity. Naturally infected squirrel monkeys exhibited long-lasting, virus-specific cell-mediated immunity in a lymphocyte proliferation assay, whereas such reactivity could not be demonstrated either in chronically infected owl monkeys or in an owl monkey with a primary H. saimiri infection. The failure of owl monkeys to respond to viral antigens was not due to a basic immunological defect, since these animals gave normal responses to heterologous cells and were capable of being sensitized with the protein antigen keyhole limpet hemocyanin.