Antibody reactions to herpesvirus saimiri (HVS)-induced early and late antigens (EA and LA) in HVS-infected squirrel, marmoset and owl monkeys

Vero cells were infected with Herpesvirus saimiri. Early (EA) and late (LA) viral antigens were distinguished by inhibiting viral DNA synthesis with cytosine arabinoside (Ara C), or allowing it to proceed uninhibited until CPE was visible. The difference in the antigenic specificity of EA and LA was confirmed by direct fluorescence tests, in combination with blocking experiments. Sera that were anti-EA positive according to the indirect test were capable of blocking the EA staining reaction with direct EA+- conjugates, whereas anti-LA+EA— sera were unable to do so. Healthy adult squirrel monkeys had antibodies to late antigens (LA) but not to early antigens (EA), as judged by immunofluorescence tests. Isolation-reared, antibody-free squirrel monkeys responded with anti-EA and anti-LA antibodies after HVS inoculation. Uninoculated, cage-mate squirrel monkeys became infected by horizontal transmission and responded with LA and EA antibodies approximately 2 months after being housed together with the infected animals. Simultaneously isolated controls remained antibody-free. HVS-inoculated, tumor-bearing marmoset and owl monkeys developed antibodies to both LA and EA in the majority of the cases studied, although in some owl monkeys there was only LA and no EA antibody development. Two different patterns of EA staining could be distinguished, trabecular and punctate. There was a conspicuous difference between the species with regard to the timing of antibody development. Squirrel monkeys, the natural host species of the virus, but resistant to its oncogenic action, responded with antibody development within 14–17 days after inoculation. Marmoset and owl monkeys did not respond until 28–80 days. Conceivably, the natural host species has been selected for a high degree of genetic responsiveness against virus-determined antigens. This may be partly or entirely responsible for its resistance to the oncogenic effect of this virus.