Depletion of total hemolytic complement in sera from hamsters bearing herpes simplex type 2-induced tumors.

Total hemolytic complement (CH50) levels were compared in sera from normal hamsters and hamsters bearing tumors derived from herpes simplex virus type 2-transformed cells CH50 in normal sera ranged from 160 to 212 while CH50 in tumor bearer sera ranged from 82 to 146. Preincubation of tumor bearer sera with cell surface proteins (CSP) from homologous herpes simplex virus type 2-derived tumor cells resulted in a 66% depletion of CH50 whereas preincubation with heterologous herpes simplex virus type 1-derived tumor CSP resulted in a decrease of 26%. The depletion of CH50 appeared to occur via the classic complement pathway. Similar results were seen using CSP from herpes simplex virus-infected cells although overall depletion of CH50 was considerably less than that seen using tumor cell material. Using the complement subcomponent 1q(C1q)-binding test, tumor bearer sera and tumor bearer sera preincubated with homologous CSP were shown to contain increased levels of immune complexes not present in normal serum. These results indicate that the observed depletion of complement activity in sera from tumor-bearing hamsters could be the result of complement pathway activation by antigen-antibody complexes.