AUTO-ANTIBODY DEPENDENT ACTIVATION OF THE AUTOLOGOUS CLASSICAL COMPLEMENT PATHWAY BY GUINEA-PIG RED-CELLS TREATED WITH INFLUENZA-VIRUS OR NEURAMINIDASE - INVITRO AND INVIVO STUDY

Abstract

Guinea pig erythrocytes that had been exposed to influenza A virus or Vibrio cholerae neuraminidase activated the classical complement pathway in autologous serum. Because all viral particles were eluted from the treated cells, activation was not dependent on antiviral antibodies or on the particles themselves. After a threshold of 45-55% desialation, had been reached, the relative capacity of treated cells to activate complement increased very rapidly with desialation. Desialation unmasked sites on which natural auto-antibodies of the IgM class were fixed. Antibody fixation on the membrane led to complement component C3b deposition on the cell membrane and activation of the classical complement sequence then cell lysis. The relevance of in vitro lysis of desialated cells to in vivo clearance of these cells is not certain because C4-deficient guinea pigs were able to eliminate desialated cells from the blood stream as efficiently as did normal guinea pigs. Membrane desialation occurring during myxovirus infection could lead to autoimmunity and tissue changes, as well as to recovery by eliminating virus-modified cells.