Viktor A. Bokisch

The Potential Pathogenic Role of Complement in Dengue Hemorrhagic Shock Syndrome

Abstract In Bangkok, Thailand, 49 of 127 patients with dengue hemorrhagic fever experienced shock. The concentration of nine complement proteins measured in serial serum samples decreased during shock with the exception of C9. C3 and C5 were reduced to 20 to 40 per cent of normal in severe cases. Decrease of plasma fibrinogen, appearance of fibrinogen split products and thrombocytopenia indicated occurence of intravascular coagulation. Metabolic studies of C3 and C1q, performed on 24 patients, indicated a markedly enhanced fractional catabolic rate especially during shock. These results support the concept that activation of complement can constitute a major factor in the pathogenesis of dengue hemorrhagic shock. (N Engl J Med 289:996–1000, 1973)

Subacute sclerosing panencephalitis: Destruction of human brain cells by antibody and complement in an autologous system

Abstract Cultured cells from the brain of a patient with subacute sclerosing panencephalitis (SSPE), a disease associated with chronic measles virus infection, were lysed by that patients own serum. Lysis was dependent on the presence of antibody(s) to measles virus and complement. Lysis, which occurred only when measles viral antigens were expressed on the cell surface, could be induced by sera and cerebral spinal fluid (CSF) from other patients with SSPE, sera from patients who had convalesced from normal measles virus infection, and heterologous rabbit serum against measles virus. Further, complement-binding immune complexes were found in the sera and CSF of patients with SSPE. These studies clearly document that patients with SSPE contain a functioning humoral attack system against cells expressing surface measles virus antigens.