{"title":"Sendai virus haemolysis: mechanism of the increased haemolysis obtained by pretreatment of the virus with antibody and complement.","authors":"P Fadnes, G Haukenes","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Sendai virus is haemolytic against erythrocytes from various species. Pretreatment of the virus with antibody and complement (C) resulted in a sixfold increase in the haemolysis. The viral haemolysin (HL) could be inactivated by heating the virus at 37 degrees C for 5 h. HL-inactivated virus became haemolytic again when pre-treated with antibody and C. This acquired haemolytic capacity corresponded to the enhanced haemolysis shown by intact virus. It is concluded that the enhanced haemolytic activity is due to a C-mediated indirect haemolysis and is not dependent on the fusion process. The possibility of cell damage in vivo from virus-antibody-C complexes is discussed.</p>","PeriodicalId":75411,"journal":{"name":"Acta pathologica et microbiologica Scandinavica. Section C, Immunology","volume":"87C 3","pages":"223-7"},"PeriodicalIF":0.0000,"publicationDate":"1979-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acta pathologica et microbiologica Scandinavica. Section C, Immunology","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Sendai virus is haemolytic against erythrocytes from various species. Pretreatment of the virus with antibody and complement (C) resulted in a sixfold increase in the haemolysis. The viral haemolysin (HL) could be inactivated by heating the virus at 37 degrees C for 5 h. HL-inactivated virus became haemolytic again when pre-treated with antibody and C. This acquired haemolytic capacity corresponded to the enhanced haemolysis shown by intact virus. It is concluded that the enhanced haemolytic activity is due to a C-mediated indirect haemolysis and is not dependent on the fusion process. The possibility of cell damage in vivo from virus-antibody-C complexes is discussed.