Ability to activate the alternative complement pathway acquired by human and guinea-pig erythrocytes after contact with influenza virus.

Human sera exhibited a little haemolytic activity on native guinea-pig erythrocytes, but became potently cytolytic for guinea-pig erythrocytes previously incubated with influenza virus. These haemolytic activities were relevant to complement activation since chelation of Ca++ and Mg++ by EDTA prevented the haemolysis as did also previous heating of sera to 56% C. The haemolysis of native red cells was promoted by human natural antibodies against guinea-pig cellular antigens, which activated the direct pathway of complement. On the other hand, haemolysis of influenza-treated cells was produced by an activation of the alternative pathway since haemolysis occurred in conditions where the direct but not the alternative pathway was blocked. Human antibodies, however, may enhance the alternative pathway but did not trigger it. The same haemolytic phenomena was observed after removal from guinea-pig erythrocyte membrane of sialic acid residues by neuraminidase. While complement-mediated haemolysis never occurred in a homologous system, that is with virus-treated cells and sera from the same species, we noticed in that case a strong haemagglutination. This observation suggested that a species recognition prevented complement mediated haemolysis, but supported the hypothesis of a complement regulation by endogenous protein(s), the complement sequence being blocked before the apparition of the cytolytic activity. The possibility of a role for the complement in the non-specific defence against the infection and a participation to the inflammatory process through this mechanism is also discussed.