Human neutrophils and eosinophils adhere to the surface of schistosomula of Schistosoma mansoni that have been preincubated with antischistosomular sera with or without complement . Neutrophils are seen to form small (<0.5 Jim), heptalaminar and large (5-8 Am), pentalaminar fusions with the normal pentalaminar parasite surface membrane . By freeze-fracture techniques, attachment areas 5-8 Am in diameter are seen to form between neutrophils and schistosomula. These areas have three zones-an edge and two centrally located areas, one of which is rich and one of which is poor in intramembrane particles (IMPS) . The edge zone is continuous around the attachment areas and is usually composed of a skipfracture that passes out of the schistosomular outer membrane into the inner membrane . In some cases, the edge zone is made up of a string of IMPS . The IMP-rich central areas have an IMP concentration similar to that of unattached neutrophil membranes, are raised off of the surface of the schistosomulum, and have two normal schistosomular membranes underneath, indicating that they are indeed unattached . The IMP-poor central areas are composed of a fused or hybrid membrane that is continuous with the neutrophil plasma membrane but that bears the same spatial relationship to the schistosomular inner membrane that the normal outer membrane does . Similar changes are seen in samples prepared without glycerination. Eosinophils generally do not fuse with the schistosomular outer membrane but, instead, discharge their granular contents onto the surface of the schistosomula and appear to adhere to the parasite through this discharged material . It is suggested that schistosomula have a capability to fuse with mammalian cells and that this fusion proceeds from a fusion of the outer leaflets to a fusion of the bilayers, as appears also to be the case in other systems.Schistosoma mansoni presents a paradox in that adult parasites are able to survive in the bloodstream for long periods of time (years in some cases), whereas schistosomula, the larvae that develop from cercariae that have penetrated the skin, are destroyed by an antibody-dependent granulocyte reaction (31) . Two questions arise from this paradox. First, how do adult parasites avoid the immune response? One answer that has been given is that the parasites acquire host antigens, namely ABH blood group glycolipids (12), Forssman antigen (7), and components of the major histocompatibility complex (30), 46