Extended hyperimmunization of rabbits with Sindbis (SIN) or Semliki Forest (SF) viruses causes the production of antisera that are cross-reactive with virus-infected cells in antibodydependent, complement-mediated cytotoxicity assays but that do not cross-neutralize viruses in vitro. C3H/HeJ mice given y globulin fractionated from the extended hyperimmune antiserum against SIN, but not control sera, were protected from challenge by 100 LDso of SF, a virus which is in a different subgroup than SIN. All mice survived if the y globulin was given 24 hr before challenge virus and partial protection occurred if the globulin was given 24 hr after the virus. Cobra venom factor treatment of normal C3H mice challenged with SF did not reduce the protection, suggesting that complement was not involved. Methyl palmitate (40 mg/mouse) given before y globulin and virus challenge suppressed macrophage activity and reduced the level of protection 23% in females and 70% in males, Silica treatment (3 mg/mouse) reduced the protection equally in both males and females by 92%. In vitro experiments were done to test if it were possible that cross-antibody-dependent cellular cytotoxicity (ADCC) could accout for the passive crossprotection observed in this system. Cross-ADCC could be demonstrated in vitro at high dilutions of antiserum (1 :25,600). On the basis of the in vitro and in vivo results presented, we suggest that 56

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Actinomycin D injected simultaneously with sheep erythrocytes in female rats caused a delay in the immune response but had no effect on the rate or maximum amount of hemagglutinin produced. The delay was roughly proportional to the concentration of the antibiotic administered, and was up to 2 days for 75 microg in a 200-gram female rat (sublethal dose for females). The dose effect in the delay in response is consistent with the time when actinomycin would no longer be available to bind with newly synthesized DNA and when messenger-RNA production could occur. Similar results were obtained with another antigen, the enzyme beta-galactosidase, in male rats during the secondary response.

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Rabbit hyperimmune antisera against Sindbis (SIN) or Semliki Forest (SF) virus were absorbed with purified SIN virus or SIN virus-infected cells, or with SF virus or SF virus-infected cells. Residual antibody titers were determined by hemagglutination inhibition (HAI) and antibody-dependent, complement-mediated cytolysis (ADCMC) assays. It appeared that absorption with virus-infected cells removed ADCMC-detectable cross-reactive antibody much more efficiently than did absorption with either virus. HAI assays with the same absorbed antisera indicated that both virus and virus-infected cells removed HAI-detectable crossreactive antibody. On the basis of these and other data, there appeared to be a cross-reactive antigen present on virus-infected cells which was detectable by ADCMC and was distinct from the cross-reactive antigen assayed by HAI.